To see the other types of publications on this topic, follow the link: Adipocyte hormones.
Journal articles on the topic 'Adipocyte hormones'
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the top 50 journal articles for your research on the topic 'Adipocyte hormones.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.
1
Vernon, R. G. "Adipocyte studies: systems for investigating effects of growth hormone and other chronically acting hormones." Biochemical Society Transactions 28, no. 2 (February 1, 2000): 126–31. http://dx.doi.org/10.1042/bst0280126.
Full textAbstract:
Adipose tissue is very amenable to study in vitro. Collagenase digestion yields free adipocytes which usually respond well to acute stimulation/inhibition by hormones and other factors. Chronic effects of hormones are best studied using explants of adipose tissue which, from some species (e.g. sheep), can be maintained in culture for up to a week without loss of function. Alternatively, pre-adipocytes can be readily isolated from adipose tissue and induced to proliferate and differentiate in culture, while various adipocyte-like cell-lines have been established, which can be used for chronic studies. Use of these various systems for investigating the mechanisms of action of growth hormone are described.
2
Lafontan, Max. "FAT CELLS: Afferent and Efferent Messages Define New Approaches to Treat Obesity." Annual Review of Pharmacology and Toxicology 45, no. 1 (September 22, 2005): 119–46. http://dx.doi.org/10.1146/annurev.pharmtox.45.120403.095843.
Full textAbstract:
For a long time neural and endocrine messages were studied for their impact on adipocyte metabolism and control of storage/release of fatty acids. In fact, bidirectional communication exists between adipocytes and other tissues. Several molecules secreted from adipocytes are involved in fat cell signaling to other tissues. Adipocyte products could initiate antagonistic effects on target tissues. Fat cells produce peptides that can elicit insulin resistance, such as tumor necrosis factor-α and resistin, as well as hormones that can improve insulin resistance, such as leptin and adiponectin. Secretion of complement proteins, proinflammatory cytokines, procoagulant, and acute phase reactant proteins have also been observed in adipocytes. There is much to learn about how these signals function. It is unlikely that all the adipocyte's endocrine and paracrine signals have been identified. Putative pharmacological strategies aiming at modulation of afferent and efferent fat cell messages are reviewed and discussed.
3
Phillips, Kevin J. "Beige Fat, Adaptive Thermogenesis, and Its Regulation by Exercise and Thyroid Hormone." Biology 8, no. 3 (July 31, 2019): 57. http://dx.doi.org/10.3390/biology8030057.
Full textAbstract:
While it is now understood that the proper expansion of adipose tissue is critically important for metabolic homeostasis, it is also appreciated that adipose tissues perform far more functions than simply maintaining energy balance. Adipose tissue performs endocrine functions, secreting hormones or adipokines that affect the regulation of extra-adipose tissues, and, under certain conditions, can also be major contributors to energy expenditure and the systemic metabolic rate via the activation of thermogenesis. Adipose thermogenesis takes place in brown and beige adipocytes. While brown adipocytes have been relatively well studied, the study of beige adipocytes has only recently become an area of considerable exploration. Numerous suggestions have been made that beige adipocytes can elicit beneficial metabolic effects on body weight, insulin sensitivity, and lipid levels. However, the potential impact of beige adipocyte thermogenesis on systemic metabolism is not yet clear and an understanding of beige adipocyte development and regulation is also limited. This review will highlight our current understanding of beige adipocytes and select factors that have been reported to elicit the development and activation of thermogenesis in beige cells, with a focus on factors that may represent a link between exercise and ‘beiging’, as well as the role that thyroid hormone signaling plays in beige adipocyte regulation.
4
Burrell, Jasmine A., Anik Boudreau, and Jacqueline M. Stephens. "Latest advances in STAT signaling and function in adipocytes." Clinical Science 134, no. 6 (March 2020): 629–39. http://dx.doi.org/10.1042/cs20190522.
Full textAbstract:
Abstract Adipocytes and adipose tissue are not inert and make substantial contributions to systemic metabolism by influencing energy homeostasis, insulin sensitivity, and lipid storage. In addition to well-studied hormones such as insulin, there are numerous hormones, cytokines, and growth factors that modulate adipose tissue function. Many endocrine mediators utilize the JAK–STAT pathway to mediate dozens of biological processes, including inflammation and immune responses. JAKs and STATs can modulate both adipocyte development and mature adipocyte function. Of the seven STAT family members, four STATs are expressed in adipocytes and regulated during adipogenesis (STATs 1, 3, 5A, and 5B). These STATs have been shown to play influential roles in adipose tissue development and function. STAT6, in contrast, is highly expressed in both preadipocytes and mature adipocytes, but is not considered to play a major role in regulating adipose tissue function. This review will summarize the latest research that pertains to the functions of STATs in adipocytes and adipose tissue.
5
Ahima, Rexford S. "Central actions of adipocyte hormones." Trends in Endocrinology & Metabolism 16, no. 7 (September 2005): 307–13. http://dx.doi.org/10.1016/j.tem.2005.07.010.
Full text
6
Vannucci, S. J., C. M. Klim, L. F. Martin, and K. F. LaNoue. "A1-adenosine receptor-mediated inhibition of adipocyte adenylate cyclase and lipolysis in Zucker rats." American Journal of Physiology-Endocrinology and Metabolism 257, no. 6 (December 1, 1989): E871—E878. http://dx.doi.org/10.1152/ajpendo.1989.257.6.e871.
Full textAbstract:
Hormone-stimulated lipolysis is reduced in genetically obese rodents and may contribute to the increased adiposity characteristic of the obese state. Endogenously released adenosine, acting via the A1 receptor coupled to the inhibitory guanosine 5'-triphosphate binding protein, Gi, provides a tonic inhibition of lipolysis in rat adipocytes. Removal of this inhibition by the addition of adenosine deaminase frequently results in maximal lipolytic activity. Adipocytes isolated from lean Zucker (Fa/?) rats responded normally to adenosine deaminase, where lipolysis in adipocytes from obese Zucker (fa/fa) rats remained approximately 50% inhibited. Adipocyte adenylate cyclase was equally responsive to activation by forskolin, but lipolytic hormones were significantly less effective in stimulating adenosine 3',5'-cyclic monophosphate (cAMP) production in the obese adipocytes. These cells also exhibited an increased sensitivity to inhibition by the adenosine agonist, N6-(L-2-phenylisopropyl)-adenosine, either in combination with forskolin or beta-adrenergic hormone stimulation. Treatment of isolated adipocytes with pertussis toxin, which uncouples receptor-mediated Gi function, had little effect in cells from lean rats but increased isoproterenol stimulated cAMP production of cells from obese rats to levels observed in the lean cells. In addition, the adenosine A1 antagonist, 8-phenyltheophylline, increased cAMP and lipolytic activity in the obese adipocytes while having little significant effect in the lean adipocytes. These results suggest that hormonal control of lipolysis is altered in the obese Zucker rat because of an alteration in A1-adenosine receptor-mediated inhibition of adenylate cyclase.
7
GREGOIRE, FRANCINE M., CYNTHIA M. SMAS, and HEI SOOK SUL. "Understanding Adipocyte Differentiation." Physiological Reviews 78, no. 3 (January 7, 1998): 783–809. http://dx.doi.org/10.1152/physrev.1998.78.3.783.
Full textAbstract:
Gregoire, Francine M., Cynthia M. Smas, and Hei Sook Sul. Understanding Adipocyte Differentiation. Physiol. Rev. 78: 783–809, 1998. — The adipocyte plays a critical role in energy balance. Adipose tissue growth involves an increase in adipocyte size and the formation of new adipocytes from precursor cells. For the last 20 years, the cellular and molecular mechanisms of adipocyte differentiation have been extensively studied using preadipocyte culture systems. Committed preadipocytes undergo growth arrest and subsequent terminal differentiation into adipocytes. This is accompanied by a dramatic increase in expression of adipocyte genes including adipocyte fatty acid binding protein and lipid-metabolizing enzymes. Characterization of regulatory regions of adipose-specific genes has led to the identification of the transcription factors peroxisome proliferator-activated receptor-γ (PPAR-γ) and CCAAT/enhancer binding protein (C/EBP), which play a key role in the complex transcriptional cascade during adipocyte differentiation. Growth and differentiation of preadipocytes is controlled by communication between individual cells or between cells and the extracellular environment. Various hormones and growth factors that affect adipocyte differentiation in a positive or negative manner have been identified. In addition, components involved in cell-cell or cell-matrix interactions such as preadipocyte factor-1 and extracellular matrix proteins are also pivotal in regulating the differentiation process. Identification of these molecules has yielded clues to the biochemical pathways that ultimately result in transcriptional activation via PPAR-γ and C/EBP. Studies on the regulation of the these transcription factors and the mode of action of various agents that influence adipocyte differentiation will reveal the physiological and pathophysiological mechanisms underlying adipose tissue development.
8
Rondinone, Cristina M. "Adipocyte-Derived Hormones, Cytokines, and Mediators." Endocrine 29, no. 1 (2006): 81–90. http://dx.doi.org/10.1385/endo:29:1:81.
Full text
9
Faraj, May, Hui Ling Lu, and Katherine Cianflone. "Diabetes, lipids, and adipocyte secretagogues." Biochemistry and Cell Biology 82, no. 1 (February 1, 2004): 170–90. http://dx.doi.org/10.1139/o03-078.
Full textAbstract:
That obesity is associated with insulin resistance and type II diabetes mellitus is well accepted. Overloading of white adipose tissue beyond its storage capacity leads to lipid disorders in non-adipose tissues, namely skeletal and cardiac muscles, pancreas, and liver, effects that are often mediated through increased non-esterified fatty acid fluxes. This in turn leads to a tissue-specific disordered insulin response and increased lipid deposition and lipotoxicity, coupled to abnormal plasma metabolic and (or) lipoprotein profiles. Thus, the importance of functional adipocytes is crucial, as highlighted by the disorders seen in both "too much" (obesity) and "too little" (lipodystrophy) white adipose tissue. However, beyond its capacity for fat storage, white adipose tissue is now well recognised as an endocrine tissue producing multiple hormones whose plasma levels are altered in obese, insulin-resistant, and diabetic subjects. The consequence of these hormonal alterations with respect to both glucose and lipid metabolism in insulin target tissues is just beginning to be understood. The present review will focus on a number of these hormones: acylation-stimulating protein, leptin, adiponectin, tumour necrosis factor α, interleukin-6, and resistin, defining their changes induced in obesity and diabetes mellitus and highlighting their functional properties that may protect or worsen lipid metabolism.Key words: C3adesarg, fatty acid trapping, lipolysis, lipogenesis.
10
Hernandez, Arturo, Bibian Garcia, and Maria-Jesus Obregon. "Gene Expression from the Imprinted Dio3 Locus Is Associated with Cell Proliferation of Cultured Brown Adipocytes." Endocrinology 148, no. 8 (August 1, 2007): 3968–76. http://dx.doi.org/10.1210/en.2007-0029.
Full textAbstract:
Active thyroid hormones are critical for the differentiation and function of brown adipose tissue. However, we have observed high basal and induced levels of type 3 deiodinase (D3), an enzyme that inactivates thyroid hormones and is coded by the imprinted gene Dio3, in differentiating brown preadipocytes in primary culture. We find that D3 activity and mRNA expression strongly correlate with the rate of proliferation of undifferentiated precursor cells under various conditions. Furthermore, differentiation of precursor cells to adipocytes is associated with decreased levels of D3 expression, and only very low levels of D3 mRNA are found in mature adipocytes. Dlk1, an inhibitor of adipocyte differentiation and a paternally expressed gene located in the same imprinted domain as Dio3, displayed changes in expression that parallel those of Dio3. In contrast, a 4-kb transcript for Dio3os, an antisense gene also located in the same imprinted domain, is markedly up-regulated in differentiated adipocytes. We conclude that D3 expression in differentiating preadipocytes is primarily linked to proliferating cells, whereas Dio3os expression is associated with mature adipocytes. Our results suggest that genomic imprinting and gene expression at the Dlk1/Dio3 imprinted domain may play a role in the regulation of adipocyte proliferation and differentiation.
11
Rochon, L., and L. J. Bukowiecki. "Alterations in adipocyte response to lipolytic hormones during cold acclimation." American Journal of Physiology-Cell Physiology 258, no. 5 (May 1, 1990): C835—C840. http://dx.doi.org/10.1152/ajpcell.1990.258.5.c835.
Full textAbstract:
The effects of cold exposure (7 days, 5 degrees C) and cold acclimation (21 days, 5 degrees C) on the regulation of lipolysis were investigated in adipocytes isolated from epididymal fat pads of rats. Catecholamines stimulated lipolysis in an affinity sequence typical of the beta 1-adrenoceptor subtype: one-half maximum velocity (1/2 Vmax) isoproterenol (35 nM) much greater than 1/2 Vmax norepinephrine (150 nM) approximately 1/2 Vmax epinephrine (200 nM). Cold exposure markedly decreased the sensitivity (1/2 Vmax) and the responsiveness (Vmax) of the adipocytes to the lipolytic action of catecholamines. Addition of adenosine deaminase to fat cells isolated from cold-exposed rats did not normalize the lipolytic activity, suggesting that extracellular adenosine was not responsible for the obtunded lipolysis. This effect of cold exposure was transient as the lipolytic response to catecholamines was normal in fully cold-acclimated animals. Remarkably, the responsiveness of adipocytes to the lipolytic action of glucagon (200 nM) and adrenocorticotropic hormone (ACTH, 1 microM) progressively increased during cold acclimation. Adipocyte lipolytic response to dibutyryl adenosine 3',5'-cyclic monophosphate (cAMP) and theophylline was normal in cold-exposed rats, indicating that the lipolytic defect resides at an early step in the lipolytic cascade (pre-cAMP). On the other hand, the antilipolytic effect of insulin on norepinephrine-induced lipolysis significantly decreased during cold acclimation, particularly at physiological levels of insulin (nanomolar level). These results demonstrate that the transient decrease in the lipolytic action of catecholamines observed during cold acclimation is compensated by 1) an increased responsiveness of adipocytes to glucagon and ACTH and 2) by a decreased effectiveness of insulin to induce antilipolysis.(ABSTRACT TRUNCATED AT 250 WORDS)
12
Wahrenberg, H., P. Engfeldt, J. Bolinder, and P. Arner. "Acute adaptation in adrenergic control of lipolysis during physical exercise in humans." American Journal of Physiology-Endocrinology and Metabolism 253, no. 4 (October 1, 1987): E383—E390. http://dx.doi.org/10.1152/ajpendo.1987.253.4.e383.
Full textAbstract:
During prolonged exercise, the free fatty acids derived from adipocyte lipolysis are the principal fuel utilized by muscles. In humans, the lipid mobilization from adipose tissue is mainly regulated by insulin and catecholamines: the latter hormones have both beta-adrenergic stimulatory and alpha 2-adrenergic inhibitory effects on lipolysis. The aim of this study was to determine whether rapid alterations in the peripheral action of the regulatory hormones occur during physical work and whether they are of importance for the enhanced lipid mobilization. The acute effects of exercise on the regulation of lipolysis were investigated in isolated adipocytes removed from the gluteal region of 14 healthy volunteers before and immediately after the exercise period. Exercise induced a 20-35% significant increase in the lipolytic response to noradrenaline alone and in combination with the selective alpha 2-antagonist yohimbine and to the pure beta-agonist isoproterenol in isolated adipocytes. The antilipolytic effects of both the alpha 2-agonist clonidine and insulin were unaffected by exercise. Exercise did not influence the specific adipocyte receptor binding of 125I-cyanopindolol (beta-adrenergic receptor), [3H]yohimbine (alpha-adrenergic receptor), and mono-125I-[Tyr A14]insulin (insulin receptor). In conclusion, a single period of submaximal exercise increases adipocyte lipolytic responsiveness to catecholamines through an increased beta-adrenoceptor-mediated effect at steps distal to the receptor binding. Thus the increased peripheral action of catecholamines may be of importance for the observed enhanced lipid mobilization during physical work.
13
Berg, Anders H., Ying Lin, Michael P. Lisanti, and Philipp E. Scherer. "Adipocyte differentiation induces dynamic changes in NF-κB expression and activity." American Journal of Physiology-Endocrinology and Metabolism 287, no. 6 (December 2004): E1178—E1188. http://dx.doi.org/10.1152/ajpendo.00002.2004.
Full textAbstract:
The adipocyte exerts an important role in energy homeostasis, both as depot for energy-rich triglycerides and as a source for metabolic hormones. Adipocytes also contribute to inflammation and the innate immune response. Although it can be physiologically beneficial to combine these two functions in a single cell type under some circumstances, the proinflammatory signals emanating from adipocytes in the obese state can have local and systemic effects that promote atherosclerosis and insulin resistance. The transcriptional machinery in the adipocyte that mediates these pro-inflammatory responses has remained poorly characterized to date. In particular, no information is currently available on the NF-κB family of transcription factors. Here, we show that adipogenesis is associated with changes in amount and subunit composition of the NF-κB complexes. NF-κB subunits p65 (RelA), p68 (RelB), and IκB are upregulated during fat cell differentiation. Correspondingly, basal NF-κB nuclear gel shift and luciferase reporter assays are induced in parallel during differentiation. Surprisingly, endotoxin sensitivity of the classical NF-κB pathway is substantially delayed and attenuated despite increased overall inflammatory response in the mature adipocyte, as judged by induction of IL-6 and TNF-α. As a reflection of the constitutively elevated NF-κB activity in the mature adipocyte, adipocytes (but not preadipocytes) exert a strong inflammatory stimulus on macrophages in vitro, suggesting a cross talk between adipocytes and interstitial macrophages in adipose tissue in vivo. These effects are mediated by a secretory product of adipocytes that is unlikely to be IL-6 or TNF-α.
14
Omatsu-Kanbe, Mariko, Kazuko Inoue, Yusuke Fujii, Takefumi Yamamoto, Takahiro Isono, Norihisa Fujita, and Hiroshi Matsuura. "Effect of ATP on preadipocyte migration and adipocyte differentiation by activating P2Y receptors in 3T3-L1 cells." Biochemical Journal 393, no. 1 (December 12, 2005): 171–80. http://dx.doi.org/10.1042/bj20051037.
Full textAbstract:
The effect of extracellular ATP on adipogenesis was investigated using the mouse 3T3-L1 cell line. Incubation of cells with ATP (1–100 μM) for 5 min induced actin filament reorganization and membrane ruffling mediated through P2Y receptors. Enhancement of preadipocyte migration into fat cell clusters is one of the essential processes of adipose tissue development in vivo and cell migration assays revealed that stimulation of P2Y receptors enhanced chemokinesis (migration) in a concentration dependent manner. In this cell line, growth arrest is required before initiation of differentiation and growth-arrested post-confluent cells can be converted into adipocytes by the presence of the adipogenic hormones dexamethasone, 3-isobutyl-1-methylxanthine and insulin. On the other hand, those hormones alone do not trigger differentiation in proliferating cells. ATP did not induce differentiation when applied alone to either proliferating or postconfluent cells. By contrast, proliferating cells (density <50%) preincubated with ATP for 5 min and subsequently given the adipogenic hormones in the continued presence of ATP, underwent adipocyte differentiation mediated through phospholipase C-coupled P2Y receptors. These adipocytes were found to show very similar characteristics, including morphology and intracellular triacylglycerol accumulation compared with adipocytes differentiated from post-confluent preadipocytes with those adipogenic hormones. When proliferating cells were preincubated with ATP before the addition of the adipogenic hormones, gene expression of aP2 (adipose protein 2) was markedly increased within 6 days, whereas without ATP pretreatment the expression level stayed very low. These results suggest that extracellular ATP renders preadipocytes responsive to adipogenic hormones during the growth phase.
15
Valdemarsson, Stig, Birger Fagher, Pavo Hedner, Mario Monti, and Peter Nilsson-Ehle. "Platelet and adipocyte thermogenesis in hypothyroid patients: a microcalorimetric study." Acta Endocrinologica 108, no. 3 (March 1985): 361–66. http://dx.doi.org/10.1530/acta.0.1080361.
Full textAbstract:
Abstract. Direct microcalorimetry was used for measurements of heat production in cell suspensions of platelets and adipocytes, obtained from hypothyroid patients before and after 3 months on full l-thyroxine substitution. Platelet heat production was significantly lower than normal before treatment and increased in all 10 patients studied; the mean value increased from 51.3 ± 1.6 fW/cell before to 57.1 ± 1.8 fW/cell after therapy (P< 0.001). Similarily, adipocyte heat production was initially significantly lower than normal and increased during treatment in all 6 patients investigated. The mean value for heat production per adipocyte was 18.8 ± 1.7 pW/cell before and 32.4 ± 2.5 pW/cell after therapy (P < 0.025), which is still below the level recorded in lean healthy subjects. The adipocyte size did not change significantly. The increase in adipocyte heat production was correlated to the increase in S-triiodothyronine levels (r = 0.84, P <0.05). In hypothyroidism, the total metabolic activity seems to be comparatively more reduced in adipocytes than in platelets. A difference may exist between these cells with regard to recovery of normal metabolic acitivity during treatment for hypothyroidism. Direct microcalorimetry appears to be an adequate method for monitoring net metabolic effects of thyroid hormones in these cells.
16
Luong, Quyen, Jun Huang, and Kevin Y. Lee. "Deciphering White Adipose Tissue Heterogeneity." Biology 8, no. 2 (April 11, 2019): 23. http://dx.doi.org/10.3390/biology8020023.
Full textAbstract:
Adipose tissue not only stores energy, but also controls metabolism through secretion of hormones, cytokines, proteins, and microRNAs that affect the function of cells and tissues throughout the body. Adipose tissue is organized into discrete depots throughout the body, and these depots are differentially associated with insulin resistance and increased risk of metabolic disease. In addition to energy-dissipating brown and beige adipocytes, recent lineage tracing studies have demonstrated that individual adipose depots are composed of white adipocytes that are derived from distinct precursor populations, giving rise to distinct subpopulations of energy-storing white adipocytes. In this review, we discuss this developmental and functional heterogeneity of white adipocytes both between and within adipose depots. In particular, we will highlight findings from our recent manuscript in which we find and characterize three major subtypes of white adipocytes. We will discuss these data relating to the differences between subcutaneous and visceral white adipose tissue and in relationship to previous work deciphering adipocyte heterogeneity within adipose tissue depots. Finally, we will discuss the possible implications of adipocyte heterogeneity may have for the understanding of lipodystrophies.
17
McHale, Matthew J., Zaheer U. Sarwar, Damon P. Cardenas, Laurel Porter, Anna S. Salinas, Joel E. Michalek, Linda M. McManus, and Paula K. Shireman. "Increased fat deposition in injured skeletal muscle is regulated by sex-specific hormones." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 302, no. 3 (February 1, 2012): R331—R339. http://dx.doi.org/10.1152/ajpregu.00427.2011.
Full textAbstract:
Sex differences in skeletal muscle regeneration are controversial; comparisons of regenerative events between sexes have not been rigorously defined in severe injury models. We comprehensively quantified inflammation and muscle regeneration between sexes and manipulated sex-specific hormones to determine effects on regeneration. Cardiotoxin injury was induced in intact, castrated and ovariectomized female and male mice; ovariectomized mice were replaced with low- or high-dose 17-β estradiol (E2) or progesterone (P4). Extent of injury was comparable between intact mice, but females were more efficient in removal of necrotic debris, despite similar tissue levels of inflammatory cells and chemokines. Myofiber size during regeneration was equivalent between intact mice and after castration or ovariectomy (OVX) but was decreased ( P < 0.001) in ovariectomized mice with high-dose E2 replacement. Intermuscular adipocytes were absent in uninjured muscle, whereas adipocyte area was increased among regenerated myofibers in all groups. Interestingly, intermuscular fat was greater ( P = 0.03) in intact females at day 14 compared with intact males. Furthermore, castration increased ( P = 0.01) and OVX decreased adipocyte accumulation. After OVX, E2, but not P4, replacement decreased ( P ≤ 0.03) fat accumulation. In conclusion, sex-dependent differences in regeneration consisted of more efficient removal of necrosis and increased fat deposition in females with similar injury, inflammation, and regenerated myofiber size; high-dose E2 decreased myofiber size and fat deposition. Adipocyte accumulation in regenerating muscle was influenced by sex-specific hormones. Recovery following muscle injury was different between males and females, and sex-specific hormones contributed to these differences, suggesting that sex-specific treatments could be beneficial after injury.
18
Flint, David J., Nadine Binart, Stephanie Boumard, John J. Kopchick, and Paul Kelly. "Developmental aspects of adipose tissue in GH receptor and prolactin receptor gene disrupted mice: site-specific effects upon proliferation, differentiation and hormone sensitivity." Journal of Endocrinology 191, no. 1 (October 2006): 101–11. http://dx.doi.org/10.1677/joe.1.06939.
Full textAbstract:
Direct metabolic effects of GH on adipose tissue are well established, but effects of prolactin (PRL) have been more controversial. Recent studies have demonstrated PRL receptors on adipocytes and effects of PRL on adipose tissue in vitro. The role of GH in adipocyte proliferation and differentiation is also controversial, since GH stimulates adipocyte differentiation in cell lines, whereas it stimulates proliferation but inhibits differentiation of adipocytes in primary cell culture. Using female gene disrupted (ko) mice, we showed that absence of PRL receptors (PRLRko) impaired development of both internal and s.c. adipose tissue, due to reduced numbers of adipocytes, an effect differing from that of reduced food intake, where cell volume is decreased. In contrast, GHRko mice exhibited major decreases in the number of internal adipocytes, whereas s.c. adipocyte numbers were increased, even though body weight was decreased by 40–50%. The changes in adipose tissue in PRLRko mice appeared to be entirely due to extrinsic factors since preadipocytes proliferated and differentiated in similar fashion to wild-type animals in vitro and their response to insulin and isoproterenol was similar to wild-type animals. This contrasted with GHRko mice, where s.c. adipocytes proliferated, differentiated, and responded to hormones in identical fashion to controls, whereas parametrial adipocytes exhibited markedly depressed proliferation and differentiation potential and failed to respond to insulin or noradrenaline. Our results provide in vivo evidence that both GH and PRL stimulate differentiation of adipocytes but that the effects of GH are site specific and induce intrinsic changes in the precursor population, which are retained in vitro.
19
Ivkovic-Lazar, Tatjana. "Development and differentiation of adipose tissue." Medical review 56, no. 3-4 (2003): 142–45. http://dx.doi.org/10.2298/mpns0304142i.
Full textAbstract:
Introduction For years adipose tissue has been considered inert, serving only as a depot of energy surplus. However, there have been recent changes, undoubtedly due to advancement of methods for studying the morphology and metabolic activities of adipose tissue (microdialysis and adipose tissue catheterization). In normal-weight subjects, adipose tissue makes 10-12% with males and 15-20% with females. About 80 % of adipose tissue is located under the skin, and the rest envelops the internal organs. With humans there are white and brown adipose tissues, which is predominant with infants and small children. Histologic characteristics From a histological point of view, it is a special form of reticular connective tissue, which contains adipocytes with netlike structure. Human adipose tissue has four types of adrenergic receptors with different topographic dispositions, which manifest different metabolic activity of adipocytes of particular body organs. Changes in adipose tissue are associated with the process of adipocyte differentiation. Critical moments for this process are last months of pregnancy, the first six months of infancy and then puberty. However, the differentiation process may also begin during maturity. Namely, as size of adipocytes can increase to a certain limit, this process can be activated after reaching a 'critical' adipocyte volume. The differentiation process is affected by a number of hormones (insulin, glucagon, corticosteroids, somatotropin (STH), thyroid gland hormones, prolactin, testosterone), but also by some other substances (fatty acids, prostaglandins, liposoluble vitamins, butyrate, aspirin, indomethacin, metylxanthine, etc.).
20
Wauters, M., RV Considine, and LF Van Gaal. "Human leptin: from an adipocyte hormone to an endocrine mediator." European Journal of Endocrinology 143, no. 3 (September 1, 2000): 293–311. http://dx.doi.org/10.1530/eje.0.1430293.
Full textAbstract:
Leptin is a mainly adipocyte-secreted protein that was discovered 5 years ago. Most of the research following this discovery focused on the role of leptin in body weight regulation, aiming to illuminate the pathophysiology of human obesity. However, more and more data are emerging that leptin is not only important in the regulation of food intake and energy balance, but that it also has a function as a metabolic and neuroendocrine hormone. It is now clear that it is especially involved in glucose metabolism, as well as in normal sexual maturation and reproduction. Besides this, interactions with the hypothalamic-pituitary-adrenal, thyroid and GH axes and even with haematopoiesis and the immune system have also been described. It has been shown that leptin secretion by the adipocyte is partly regulated by other hormones, such as insulin, cortisol, and sex steroids, mainly testosterone. Also, other hormones like thyroid hormone and GH are possibly involved in leptin synthesis. Leptin itself exerts effects on different endocrine axes, mainly on the hypothalamic-pituitary-gonadal axis and on insulin metabolism, but also on the hypothalamic-pituitary-adrenal, thyroid and GH axes. Leptin may thus be considered a new endocrine mediator, besides its obvious role in body weight regulation.
21
Jackson, Malaka B., and Rexford S. Ahima. "Neuroendocrine and metabolic effects of adipocyte-derived hormones." Clinical Science 110, no. 2 (January 17, 2006): 143–52. http://dx.doi.org/10.1042/cs20050243.
Full textAbstract:
Obesity is characterized by an increase in adipose tissue mass. Contrary to the previous view of adipose tissue as simply an inert tissue devoted to energy storage, studies over the past decade have shown that adipose tissue is actively involved in regulating physiological processes and participates in disease. Adipose tissue secretes factors that exert local and systemic effects. Leptin, pro-inflammatory cytokines, resistin and proteins involved in haemodynamic regulation and coagulation are increased in obesity while adiponectin is reduced. The production of active corticosteroids is also increased in obesity. There is now growing evidence that adipocyte secretory factors regulate energy homoeostasis, as well as cardiovascular and immune systems. Some adipocyte hormones, most notably leptin, act in the brain to influence the neuroendocrine axis and energy balance, whereas adiponectin and resistin exert opposing effects on glucose and lipids. Understanding the actions of adipocyte hormones will provide novel insights into the pathophysiology and treatment of obesity.
22
Wilson, E. Jane, and Morley D. Hollenberg. "Effects of oxytocin and vasopressin on the preadipocyte 3T3-F442A cell line." Biochemistry and Cell Biology 65, no. 3 (March 1, 1987): 211–18. http://dx.doi.org/10.1139/o87-027.
Full textAbstract:
The 3T3-F442A mouse fibroblast cell line, triggered by factors present in fetal calf serum (FCS), converts either spontaneously or, in the simultaneous presence of FCS and insulin, at an accelerated rate into cells exhibiting the adipocyte phenotype. The effects of the neurohypophysial hormones in differentiated cells on glucose metabolism (glucose oxidation and lipogenesis) were compared with the stimulatory actions of insulin, which had its most pronounced effects in cells differentiated spontaneously with FCS in the absence of insulin. The differentiated 3T3-F442A cells were sensitive to physiological levels of insulin and exhibited manyfold increases in glucose metabolism in response to it. This result demonstrated that these cultured cells respond to insulin, in a manner analogous to freshly isolated adipocytes. In contrast to its insulin-like effects in isolated epididymal adipocytes, oxytocin was not reproducibly able to stimulate glucose metabolism in differentiated 3T3-F442A cells. Vasopressin was similarly inactive. In contrast, both oxytocin and vasopressin blocked adipocyte conversion triggered by FCS, either in the presence or absence of insulin; vasopressin was more potent than oxytocin, indicating that a vasopressin receptor was responsible for the observed inhibition of differentiation. Our work suggests that vasopressin could potentially play a role in the regulation of the adipocyte differentiation process.
23
Ahima, Rexford S. "Metabolic Actions of Adipocyte Hormones: Focus on Adiponectin." Obesity 14, no. 2S (February 2006): 9S—15S. http://dx.doi.org/10.1038/oby.2006.276.
Full text
24
Maeda, Norikazu, Tohru Funahashi, Yuji Matsuzawa, and Iichiro Shimomura. "Adiponectin, a unique adipocyte-derived factor beyond hormones." Atherosclerosis 292 (January 2020): 1–9. http://dx.doi.org/10.1016/j.atherosclerosis.2019.10.021.
Full text
25
Ros, M., J. K. Northup, and C. C. Malbon. "Adipocyte G-proteins and adenylate cyclase. Effects of adrenalectomy." Biochemical Journal 257, no. 3 (February 1, 1989): 737–44. http://dx.doi.org/10.1042/bj2570737.
Full textAbstract:
Steroid hormones modulate the ability of cells to respond to hormones that act via cyclic AMP. In adipocytes of adrenalectomized rats, cyclic AMP accumulation and lipolysis in response to adrenaline are attenuated. However, the mechanism(s) of these effects are poorly understood. The effects of altered glucocorticoid status in vivo on the steady-state amounts of components of the hormone-sensitive adenylate cyclase were analysed in rat adipocytes. beta-Adrenergic receptors were analysed by using radioligand binding and immunoblotting with an anti-receptor antiserum. Neither the amount of radioligand binding nor the amount of beta-adrenergic-receptor peptide (Mr 67,000) was altered by adrenalectomy, whereas treatment of adrenalectomized rats with dexamethasone was found to increase both parameters by more than 25% with respect to the control. Forskolin-stimulated adenylated cyclase activity was unchanged in membranes isolated from adipocytes of adrenalectomized rats, but was decreased (50%) in those from dexamethasone-treated rats. The alpha-subunit of Gs was probed by using cholera-toxin-catalysed ADP-ribosylation. Immunoblotting was used to analyse the steady-state amounts of G-protein beta-subunits (beta-G35/36). Adrenalectomy was associated with decreases in the steady-state amounts of alpha-Gs (30%) and beta-G35/36 (50%). Dexamethasone treatment of adrenalectomized animals partially restored the lipolytic response of adipocytes to adrenaline and the amounts of alpha-Gs, increased the amounts of beta-G35/36 subunits from 50% to 150% of control values, increased beta-adrenergic receptors by more than 25% and decreased adenylate cyclase activity (50%). These results suggest that the steady-state amounts of components of hormone-sensitive adenylate cyclase are differentially regulated by glucocorticoids.
26
MacLaren, R., D. Kalant, and K. Cianflone. "The ASP receptor C5L2 is regulated by metabolic hormones associated with insulin resistance." Biochemistry and Cell Biology 85, no. 1 (February 2007): 11–21. http://dx.doi.org/10.1139/o06-207.
Full textAbstract:
Acylation-stimulating protein (ASP) and interaction with its receptor C5L2 influences adipocyte metabolism. We examined insulin resistance and differentiation-mediated regulation of C5L2 and the mechanistic impact on both C5L2 cell-surface protein and ligand binding to the receptor. C5L2 mRNA increased 8.7-fold with differentiation in 3T3-L1 cells (p < 0.0001) by day 9. In preadipocytes, insulin and dexamethasone increased C5L2 mRNA (1 μmol/L insulin resulted in a 2.6-fold increase, p < 0.01; 10 nmol/L dexamethasone resulted in a 17.9-fold increase, p < 0.01) and C5L2 cell-surface protein (100 nmol insulin resulted in a 2.7-fold increase, p < 0.001; 10 nmol/L dexamethasone resulted in a 2.8-fold increase, p < 0.001). In adipocytes, 100 nmol/L insulin increased C5L2 mRNA and ASP binding (respectively, 1.3-fold, p < 0.01; and 2.4-fold, p < 0.05). Dexamethasone decreased ligand binding (–60%, p < 0.02) without changing mRNA. Tumor necrosis factor alpha decreased C5L2 mRNA (–88% in preadipocytes and –38% in adipocytes, p < 0.001), C5L2 cell-surface protein (–53% in preadipocytes, p < 0.0001), and ASP binding (–60% and –49% in, respectively, preadipocytes and adipoctyes, p < 0.05). Conversely, 1 μmol/L and 10 nmol/L rosiglitazone increased, respectively, C5L2 mRNA (9.3-fold, p < 0.0001) and ASP binding (2.4-fold, p < 0.05). Thus, C5L2 mRNA increases with differentiation, insulin, and thiazolidinedione treatment, and decreases with tumor necrosis factor alpha, all of which results in functional changes in ASP–C5L2 response and may have implications for human metabolism.
27
Boncheva, M., and T. Turnovska. "Administration of Bioflavonoides Improves Plasma Levels of Adipocyte Hormones." Acta Medica Bulgarica 41, no. 2 (December 1, 2014): 5–11. http://dx.doi.org/10.1515/amb-2014-0014.
Full textAbstract:
Summary Since time immemorial the fruits of aronia melanocarpa (rich of bioflavonoides) have been known for their medicinal properties. Present-day research of the pharmacological effects of aronia melanocarpa juice and fruits intake indicates that their high contents of anthocyanins is closely related to the health enhancing properties of this plant. This is a key fact which can be used in the prevention of most commonly spread, socially significant diseases, reducing for instance the total risk of cardio-vascular diseases. The great molecular variety anthocyanins possess and the role they play in cell metabolism, are still being investigated. This gives grounds to study the effects of Aronia melanocarpa on human cells, tissues, and organs. The aim of this study is to trace the effect of 150-200 ml aronia melanokarpa juice daily oral intake on the adipocyte hormones leptin (Lp), resistine (Rs) and adiponectin (Adn) blood levels in 10 patients with high body mass index (BMI, kg/m2) and high waist circumference. We used ELISA methods for hormonal analyses. During the study-period of two months patients did not change anything in their lifestyle. In the study group, the levels of Rs, Lp and Adn changed significantly compared to their baseline levels (averages, ng/mL) - 6.93 ± 0.137, 18.40 ±1.021 and 7.98 ± 0.077 vs. 5.06 ± 0.011, 15.23 ± 0.906 and 10.45 ± 0.103 at the end of the second month, respectively. Compared with the control group of 6 people, matched for BMI, not receiving aronia melanocarpa juice, these values were markedly different. Patients taking aronia melanokarpa juice report improvement in various conditions that have caused them discomfort before the research started: pain in the muscles and joints faded away and were replaced by a new feeling of strength, headache attacks disappeared, improvement in memory and sleep were reported, regular defecation, no signs of gastric discomfort, better vision, a quicker auditory reaction, motivation for having sex, good mood were also reported. Obese patients with insulin resistance have decreased serum adiponectin and increased serum resistin and leptin. The levels of these three hormones changed positively after chronic intake of aronia juice. We recommend a daily intake of aronia juice for the prevention of health.
28
Shinohara, Osamu, Yoh-Ichi Murata, and Makoto Shimizu. "Enhancement of differentiation of cultured adipogenic cells (TA1) by pertussis toxin." Biochemistry and Cell Biology 70, no. 8 (August 1, 1992): 650–55. http://dx.doi.org/10.1139/o92-100.
Full textAbstract:
Differentiation of adipocytes is controlled by a variety of hormones and growth factors. To investigate the possible role of GTP-binding proteins (G proteins) in the process of adipose conversion, we studied the effect of pertussis toxin on differentiation of the fibroblast/adipocyte cell line (TA1). Pertussis toxin potentiated dexamethasone- and indomethacin-induced adipocyte differentiation in a time- and dose-dependent fashion. Addition of dibutyryl cAMP or forskolin inhibited adipose conversion, indicating that an abolishment of inhibitory control of adenylate cyclase is not responsible for the action of pertussis toxin. The B oligomer of the toxin did not mimic the effect of the holotoxin. Pertussis toxin catalyzed ADP-ribosylation of 40 000 molecular mass protein of the membrane fraction was dose-dependently inhibited by the pretreatment of the cells with the toxin. These results indicate the possible involvement of pertussis toxin-sensitive G proteins in adipogenesis.Key words: adipose tissue, pertussis toxin, GTP-binding protein.
29
Unger, Roger H., Philipp E. Scherer, and William L. Holland. "Dichotomous roles of leptin and adiponectin as enforcers against lipotoxicity during feast and famine." Molecular Biology of the Cell 24, no. 19 (October 2013): 3011–15. http://dx.doi.org/10.1091/mbc.e12-10-0774.
Full textAbstract:
Science is marked by the death of dogmas; the discovery that adipocytes are more than just lipid-storing cells but rather produce potent hormones is one such example that caught physiologists by surprise and reshaped our views of metabolism. While we once considered the adipocyte as a passive storage organ for efficient storage of long-term energy reserves in the form of triglyceride, we now appreciate the general idea (once a radical one) that adipocytes are sophisticated enough to have potent endocrine functions. Over the past two decades, the discoveries of these adipose-derived factors (“adipokines”) and their mechanistic actions have left us marveling at and struggling to understand the role these factors serve in physiology and the pathophysiology of obesity and diabetes. These hormones may serve an integral role in protecting nonadipose tissues from lipid-induced damage during nutrient-deprived or replete states. As such, adipocytes deliver not only potentially cytotoxic free fatty acids but, along with these lipids, antilipotoxic adipokines such as leptin, adiponectin, and fibroblast growth factor 21 that potently eliminate excessive local accumulation of these lipids or their conversion to unfavorable sphingolipid intermediates.
30
Huang, Wan-Yu, Dar-Ren Chen, Chew-Teng Kor, Ting-Yu Chen, Po-Te Lin, Joseph Ta Chien Tseng, and Hung-Ming Wu. "Relationships between Follicle-Stimulating Hormone and Adiponectin in Postmenopausal Women." Metabolites 10, no. 10 (October 19, 2020): 420. http://dx.doi.org/10.3390/metabo10100420.
Full textAbstract:
Beyond fertility, follicle-stimulating hormone (FSH) may exert action on adipocytes, which are the major source of adiponectin and leptin, linking to insulin resistance. Therefore, we evaluated the relationships between FSH and adipocyte-derived hormones. This cross-sectional study enrolled postmenopausal women aged 40–65 years. The variables measured in this study included clinical parameters, fasting levels of sex hormones, glucose, insulin, and adipokines. A total of 261 women without breast cancer, 88 women with breast cancer receiving tamoxifen, and 59 women with breast cancer receiving additional gonadotropin-releasing hormone analogs were enrolled in this study. Significant differences in the levels of adiponectin, leptin, and FSH were observed between the non-breast cancer group and the breast cancer groups. Spearman’s rank test revealed significant associations of FSH with either body mass index (BMI) or homeostatic model assessment of insulin resistance (HOMA-IR) values in the non-breast cancer group. After adjusting for BMI, age, and menopause duration, FSH levels were significantly associated with adiponectin (p < 0.001) and the leptin-to-adiponectin ratio (p = 0.008) in the non-breast cancer group, but they were only significantly associated with adiponectin (p = 0.001) in the breast cancer group receiving tamoxifen. Our data show that FSH levels are independently associated with adiponectin levels in postmenopausal women, suggesting that adiponectin may link FSH to metabolic relationships in postmenopausal female.
31
Monjo, Marta, Esperanza Pujol, and Pilar Roca. "α2- to β3-Adrenoceptor switch in 3T3-L1 preadipocytes and adipocytes: modulation by testosterone, 17β-estradiol, and progesterone." American Journal of Physiology-Endocrinology and Metabolism 289, no. 1 (July 2005): E145—E150. http://dx.doi.org/10.1152/ajpendo.00563.2004.
Full textAbstract:
Sex steroid hormones are important factors in the determination of fat distribution and accumulation. The aim of this study was to investigate the effect of testosterone (T), 17β-estradiol (17βE), and progesterone (P) on adrenergic receptor (AR) gene expression in 3T3-L1 preadipocytes and adipocytes and their relation to the proliferation and differentiation processes. Our data clearly show that α2A-AR was the highest AR subtype expressed in preadipocytes, whereas in mature adipocytes was by far β3-AR. In the differentiation process to adipocytes, α2A-AR expression was decreased to 0.3-fold ( P < 0.01), whereas β3-AR was upregulated 578-fold ( P < 0.001) compared with preadipocytes. In addition, the expression of α2A-AR in preadipocytes was increased upon incubation with T, 17βE, and P, and a stimulation of proliferation was also observed in 17βE- and P-treated cells. In mature adipocytes, 17βE and P enhanced both α2A- and β3-AR gene expression (although the effects on β3-AR mRNA levels could be more relevant, since β3-AR was the most highly expressed), whereas T only increased α2A-AR mRNA levels. Leptin and adipocyte fatty acid-binding protein mRNA levels were higher after 17βE and P treatment, possibly indicating a proadipogenic effect of these hormones. In conclusion, this study indicates that AR gene expression is affected by these hormones in both preadipocytes and adipocytes, which could have potential importance when considering the role of ARs in the mechanisms underlying the sex-related differences in adipose tissue regional distribution.
32
Sarr, Ousseynou, Florence Gondret, Agnès Jamin, Isabelle Le Huërou-Luron, and Isabelle Louveau. "A high-protein neonatal formula induces a temporary reduction of adiposity and changes later adipocyte physiology." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 300, no. 2 (February 2011): R387—R397. http://dx.doi.org/10.1152/ajpregu.00459.2010.
Full textAbstract:
The high-protein content of formula offered to low-birth weight babies is suspected to increase the risk of obesity later in life. This study assesses the immediate and subsequent effects of a protein intake in excess during suckling on hormonal and metabolic status and adipose tissue features in a porcine model of intrauterine growth restriction. Piglets were fed milk replacers formulated to provide an adequate (AP) or a high (HP) protein supply from day 2 to day 28. A subset of piglets was killed at day 28. After weaning, the remaining piglets had free access to the same solid high-fat diet until day 160. From day 2 to day 28, HP piglets had a greater daily weight gain ( P < 0.05). Relative weight of perirenal adipose tissue (PAT), adipocyte mean diameters, activities of lipogenic enzymes in PAT and subcutaneous adipose tissue (SCAT), and leptinemia were lower ( P < 0.05) in HP piglets than in AP piglets. Genes related to glucose utilization and lipid anabolism in PAT and SCAT were ( P < 0.05) or tended ( P < 0.1) to be downregulated in HP piglets. At day 160, adipocytes were enlarged, whereas lipogenic rates in adipocytes were reduced ( P < 0.05) in SCAT of HP compared with AP pigs. Percent body fat, mRNA levels of genes controlling lipid metabolism, and plasma concentrations of hormones and metabolites were similar in HP and AP pigs. In conclusion, a HP neonatal formula induced a temporary reduction of adiposity and changed adipocyte physiology at peripubertal age.
33
Dani, C., A. G. Smith, S. Dessolin, P. Leroy, L. Staccini, P. Villageois, C. Darimont, and G. Ailhaud. "Differentiation of embryonic stem cells into adipocytes in vitro." Journal of Cell Science 110, no. 11 (June 1, 1997): 1279–85. http://dx.doi.org/10.1242/jcs.110.11.1279.
Full textAbstract:
Embryonic stem cells, derived from the inner cell mass of murine blastocysts, can be maintained in a totipotent state in vitro. In appropriate conditions embryonic stem cells have been shown to differentiate in vitro into various derivatives of all three primary germ layers. We describe in this paper conditions to induce differentiation of embryonic stem cells reliably and at high efficiency into adipocytes. A prerequisite is to treat early developing embryonic stem cell-derived embryoid bodies with retinoic acid for a precise period of time. Retinoic acid could not be substituted by adipogenic hormones nor by potent activators of peroxisome proliferator-activated receptors. Treatment with retinoic acid resulted in the subsequent appearance of large clusters of mature adipocytes in embryoid body outgrowths. Lipogenic and lipolytic activities as well as high level expression of adipocyte specific genes could be detected in these cultures. Analysis of expression of potential adipogenic genes, such as peroxisome proliferator-activated receptors gamma and delta and CCAAT/enhancer binding protein beta, during differentiation of retinoic acid-treated embryoid bodies has been performed. The temporal pattern of expression of genes encoding these nuclear factors resembled that found during mouse embryogenesis. The differentiation of embryonic stem cells into adipocytes will provide an invaluable model for the characterisation of the role of genes expressed during the adipocyte development programme and for the identification of new adipogenic regulatory genes.
34
Fasshauer, M., J. Klein, S. Krahlisch, U. Lossner, M. Klier, M. Bluher, and R. Paschke. "GH is a positive regulator of tumor necrosis factor alpha-induced adipose related protein in 3T3-L1 adipocytes." Journal of Endocrinology 178, no. 3 (September 1, 2003): 523–31. http://dx.doi.org/10.1677/joe.0.1780523.
Full textAbstract:
Tumor necrosis factor (TNF) alpha-induced adipose-related protein (TIARP) has recently been cloned as a TNFalpha-stimulated protein expressed in adipocytes. Its expression is differentiation-dependent and potentially involved in mediating TNFalpha-induced insulin resistance. To further characterize regulation of TIARP gene expression, 3T3-L1 adipocytes were treated with key hormones modulating insulin sensitivity and influencing adipocyte metabolism, and TIARP gene expression was determined by quantitative real-time RT-PCR. Interestingly, TIARP mRNA expression was stimulated almost 9-fold after 500 ng/ml GH were added for 16 h whereas addition of 10 microM isoproterenol, 100 nM insulin and 100 nM dexamethasone for 16 h significantly decreased TIARP gene expression to between 35 and 50% of control levels. In contrast, angiotensin 2 (10 microM) and triiodothyronine (1 microM) did not have any effect. The stimulatory effect of GH was time- and dose-dependent with stimulation occurring as early as 1 h after effector addition and at concentrations as low as 5 ng/ml GH. Moreover, pharmacological inhibition of Janus kinase 2 and p42/44 mitogen-activated protein kinase reversed the stimulatory effect of GH, suggesting that both signaling molecules are involved in activation of TIARP gene expression by GH. Furthermore, an increase of TIARP mRNA could be completely reversed to control levels by withdrawal of GH for 24 h. Taken together, these results show that TIARP is not only responsive to TNFalpha but also to important other hormones influencing glucose homeostasis and adipocyte metabolism. Thus, this factor may play an integrative role in the pathogenesis of insulin resistance and its link to obesity.
35
Vernon, R. G. "Adipocyte studies: systems for investigating effects of growth hormone and other chronically acting hormones." Biochemical Society Transactions 28, no. 1 (February 1, 2000): A9. http://dx.doi.org/10.1042/bst028a009b.
Full text
36
Ren, Tingting, Jinhan He, Hongfeng Jiang, Luxia Zu, Shenshen Pu, Xiaohui Guo, and Guoheng Xu. "Metformin reduces lipolysis in primary rat adipocytes stimulated by tumor necrosis factor-α or isoproterenol." Journal of Molecular Endocrinology 37, no. 1 (August 2006): 175–83. http://dx.doi.org/10.1677/jme.1.02061.
Full textAbstract:
In patients with type 2 non-insulin-dependent diabetes mellitus (NIDDM), the biguanide, metformin, exerts its antihyperglycemic effect by improving insulin sensitivity, which is associated with decreased level of circulating free fatty acids (FFA). The flux of FFA and glycerol from adipose tissue to the blood stream primarily depends on the lipolysis of triacylglycerols in the adipocytes. Adipocyte lipolysis is physiologically stimulated by catecholamine hormones. Tumor necrosis factor-α (TNF-α), a cytokine largely expressed in adipose tissue, stimulates chronic lipolysis, which may be associated with increased systemic FFA and insulin resistance in obesity and NIDDM. In this study, we examined the role of metformin in inhibiting lipolytic action upon various lipolytic stimulations in primary rat adipocytes. Treatment with metformin attenuated TNF-α-mediated lipolysis by suppressing phosphorylation of extracellular signal-related kinase 1/2 and reversing the downregulation of perilipin protein in TNF-α-stimulated adipocytes. The acute lipolytic response to adrenergic stimulation of isoproterenol was also restricted by metformin. A high concentration of glucose in the adipocyte culture promoted the basal rate of glycerol release and significantly enhanced the lipolytic action stimulated by either TNF-α or isoproterenol. Metformin not only inhibits the basal lipolysis simulated by high glucose, but also suppresses the high glucose-enhanced lipolysis response to TNF-α or isoproterenol. The antilipolytic action in adipocytes could be the mechanism by which cellular action by metformin reduces systemic FFA concentration and thus improves insulin sensitivity in obese patients and the hyperglycemic conditions of NIDDM.
37
Rajkumar, K., T. Modric, and LJ Murphy. "Impaired adipogenesis in insulin-like growth factor binding protein-1 transgenic mice." Journal of Endocrinology 162, no. 3 (September 1, 1999): 457–65. http://dx.doi.org/10.1677/joe.0.1620457.
Full textAbstract:
Differentiation of precursor cells into mature fat cells is accompanied by enhanced expression of insulin-like growth factor (IGF)-I and is stimulated by multiple hormones including growth hormone, glucocorticoids, IGF-I and insulin. We used transgenic mice that overexpress insulin-like growth factor binding protein-1 to investigate the role of IGF-I in the accumulation of fat tissue. In response to a sucrose-enriched diet, transgenic mice gained significantly less body weight and the epididymal fat mass was significantly reduced compared with wild-type mice. The increase in adipocyte size was also significantly reduced in transgenic mice compared with wild-type mice. Fewer colonies were generated from adipose tissue from transgenic mice and the mitogenic response of these cells to IGF-I was significantly reduced compared with those from wild-type mice. Induction of glycerol-3-phosphate dehydrogenase, a measure of adipocyte differentiation, by IGF-I but not insulin, was reduced in preadipocytes from transgenic mice. These data indicate that IGF-I has a critical role in the proliferation of adipocyte precursors, the differentiation of preadipocytes and the development of obesity in response to calorie excess.
38
McMillen, I. C., L. J. Edwards, J. Duffield, and B. S. Muhlhausler. "Regulation of leptin synthesis and secretion before birth: implications for the early programming of adult obesity." Reproduction 131, no. 3 (March 2006): 415–27. http://dx.doi.org/10.1530/rep.1.00303.
Full textAbstract:
A series of epidemiological, clinical and experimental studies have shown that there are associations between the fetal and neonatal nutritional environment and the amount and distribution of adipose tissue in adult life. This review considers the evidence for these relationships and discusses the potential impact of the prenatal nutritional experience on the development of the endocrine and neuroendocrine systems that regulate energy balance, with a particular emphasis on the role of the adipocyte-derived hormone, leptin. In the rodent, leptin derived from the mother may exert an important influence on the development of the appetite regulatory neural network and on the subsequent regulation of leptin synthesis and the risk for obesity in the offspring. In species such as the human and sheep, there is also recent evidence that the synthesis and secretion of adipocyte-derived hormones, such as leptin, are regulated in fetal life. Furthermore, the hypothalamic neuropeptides that regulate energy intake and expenditure in adult life are also present within the fetal brain and may be regulated by the prevailing level of maternal and hence fetal nutrient and hormonal signals, including leptin. This work is important in determining those initiating mechanisms within the ‘fat–brain’ axis in early life that precede the development of adult obesity.
39
Lafontan, Max. "Historical perspectives in fat cell biology: the fat cell as a model for the investigation of hormonal and metabolic pathways." American Journal of Physiology-Cell Physiology 302, no. 2 (January 15, 2012): C327—C359. http://dx.doi.org/10.1152/ajpcell.00168.2011.
Full textAbstract:
For many years, there was little interest in the biochemistry or physiology of adipose tissue. It is now well recognized that adipocytes play an important dynamic role in metabolic regulation. They are able to sense metabolic states via their ability to perceive a large number of nervous and hormonal signals. They are also able to produce hormones, called adipokines, that affect nutrient intake, metabolism and energy expenditure. The report by Rodbell in 1964 that intact fat cells can be obtained by collagenase digestion of adipose tissue revolutionized studies on the hormonal regulation and metabolism of the fat cell. In the context of the advent of systems biology in the field of cell biology, the present seems an appropriate time to look back at the global contribution of the fat cell to cell biology knowledge. This review focuses on the very early approaches that used the fat cell as a tool to discover and understand various cellular mechanisms. Attention essentially focuses on the early investigations revealing the major contribution of mature fat cells and also fat cells originating from adipose cell lines to the discovery of major events related to hormone action (hormone receptors and transduction pathways involved in hormonal signaling) and mechanisms involved in metabolite processing (hexose uptake and uptake, storage, and efflux of fatty acids). Dormant preadipocytes exist in the stroma-vascular fraction of the adipose tissue of rodents and humans; cell culture systems have proven to be valuable models for the study of the processes involved in the formation of new fat cells. Finally, more recent insights into adipocyte secretion, a completely new role with major metabolic impact, are also briefly summarized.
40
Lizcano, Fernando, and Guillermo Guzmán. "Estrogen Deficiency and the Origin of Obesity during Menopause." BioMed Research International 2014 (2014): 1–11. http://dx.doi.org/10.1155/2014/757461.
Full textAbstract:
Sex hormones strongly influence body fat distribution and adipocyte differentiation. Estrogens and testosterone differentially affect adipocyte physiology, but the importance of estrogens in the development of metabolic diseases during menopause is disputed. Estrogens and estrogen receptors regulate various aspects of glucose and lipid metabolism. Disturbances of this metabolic signal lead to the development of metabolic syndrome and a higher cardiovascular risk in women. The absence of estrogens is a clue factor in the onset of cardiovascular disease during the menopausal period, which is characterized by lipid profile variations and predominant abdominal fat accumulation. However, influence of the absence of these hormones and its relationship to higher obesity in women during menopause are not clear. This systematic review discusses of the role of estrogens and estrogen receptors in adipocyte differentiation, and its control by the central nervous systemn and the possible role of estrogen-like compounds and endocrine disruptors chemicals are discussed. Finally, the interaction between the decrease in estrogen secretion and the prevalence of obesity in menopausal women is examined. We will consider if the absence of estrogens have a significant effect of obesity in menopausal women.
41
Odle, Angela K., Anessa Haney, Melody Allensworth-James, Noor Akhter, and Gwen V. Childs. "Adipocyte Versus Pituitary Leptin in the Regulation of Pituitary Hormones: Somatotropes Develop Normally in the Absence of Circulating Leptin." Endocrinology 155, no. 11 (November 1, 2014): 4316–28. http://dx.doi.org/10.1210/en.2014-1172.
Full textAbstract:
Abstract Leptin is a cytokine produced by white fat cells, skeletal muscle, the placenta, and the pituitary gland among other tissues. Best known for its role in regulating appetite and energy expenditure, leptin is produced largely by and in proportion to white fat cells. Leptin is also important to the maintenance and function of the GH cells of the pituitary. This was shown when the deletion of leptin receptors on somatotropes caused decreased numbers of GH cells, decreased circulating GH, and adult-onset obesity. To determine the source of leptin most vital to GH cells and other pituitary cell types, we compared two different leptin knockout models with Cre-lox technology. The global Lep-null model is like the ob/ob mouse, whereby only the entire exon 3 is deleted. The selective adipocyte-Lep-null model lacks adipocyte leptin but retains pituitary leptin, allowing us to investigate the pituitary as a potential source of circulating leptin. Male and female mice lacking adipocyte leptin (Adipocyte-lep-null) did not produce any detectable circulating leptin and were infertile, suggesting that the pituitary does not contribute to serum levels. In the presence of only pituitary leptin, however, these same mutants were able to maintain somatotrope numbers and GH mRNA levels. Serum GH trended low, but values were not significant. However, hypothalamic GHRH mRNA was significantly reduced in these animals. Other serum hormone and pituitary mRNA differences were observed, some of which varied from previous results reported in ob/ob animals. Whereas pituitary leptin is capable of maintaining somatotrope numbers and GH mRNA production, the decreased hypothalamic GHRH mRNA and low (but not significant) serum GH levels indicate an important role for adipocyte leptin in the regulation of GH secretion in the mouse. Thus, normal GH secretion may require the coordinated actions of both adipocyte and pituitary leptin.
42
Fernández-Riejos, Patricia, Souad Najib, Jose Santos-Alvarez, Consuelo Martín-Romero, Antonio Pérez-Pérez, Carmen González-Yanes, and Víctor Sánchez-Margalet. "Role of Leptin in the Activation of Immune Cells." Mediators of Inflammation 2010 (2010): 1–8. http://dx.doi.org/10.1155/2010/568343.
Full textAbstract:
Adipose tissue is an active endocrine organ that secretes various humoral factors (adipokines), and its shift to production of proinflammatory cytokines in obesity likely contributes to the low-level systemic inflammation that may be present in metabolic syndrome-associated chronic pathologies such as atherosclerosis. Leptin is one of the most important hormones secreted by adipocytes, with a variety of physiological roles related to the control of metabolism and energy homeostasis. One of these functions is the connection between nutritional status and immune competence. The adipocyte-derived hormone leptin has been shown to regulate the immune response, innate and adaptive response, both in normal and pathological conditions. The role of leptin in regulating immune response has been assessed in vitro as well as in clinical studies. It has been shown that conditions of reduced leptin production are associated with increased infection susceptibility. Conversely, immune-mediated disorders such as autoimmune diseases are associated with increased secretion of leptin and production of proinflammatory pathogenic cytokines. Thus, leptin is a mediator of the inflammatory response.
43
Lee, Mi-Jeong, and Susan K. Fried. "Integration of hormonal and nutrient signals that regulate leptin synthesis and secretion." American Journal of Physiology-Endocrinology and Metabolism 296, no. 6 (June 2009): E1230—E1238. http://dx.doi.org/10.1152/ajpendo.90927.2008.
Full textAbstract:
This review summarizes recent advances in our understanding of the pre- and posttranscriptional mechanisms that regulate leptin production and secretion in adipocytes. Basal leptin production is proportional to the status of energy stores, i.e., fat cell size, and this is mainly regulated by alterations in leptin mRNA levels. Leptin mRNA levels are regulated by hormones, including glucocorticoids and catecholamines, but little is known about the transcriptional mechanisms involved. Leptin synthesis and secretion is also acutely modulated in response to hormones such as insulin and the availability of metabolic fuels. Acute variations in leptin production over a time course of minutes to hours are mediated at the levels of both translation and secretion. Increases in amino acids and insulin after a meal activate the mammalian target of rapamycin (mTOR) pathway, leading to an increase in specific rates of leptin biosynthesis. Cross-talk among mTOR, PKA, and AMP-activated protein kinase pathways appears to integrate hormonal and nutrient signals that regulate leptin mRNA translation, at least in part through mechanisms involving its 5′- and 3′-untranslated regions. In addition, the rate of leptin secretion from preformed stores in response to hormonal cues is also regulated. Insulin stimulates, and adrenergic agonists inhibit, leptin secretion, and this likely contributes to variations in the magnitude of nutrition-related leptin excursions and oscillations. Overall, the study of leptin production has contributed to a deepening understanding of leptin biology and, more broadly, to our understanding of the cellular and molecular mechanisms by which the adipocyte integrates hormonal and nutrient signals to regulate adipokine production.
44
Ramadoss, Sivakumar. "Inflammatory Cytokine TNF-a Controls Mesenchymal Stem Fate by Regulating JMJD3 Expression." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A235—A236. http://dx.doi.org/10.1210/jendso/bvab048.479.
Full textAbstract:
Abstract Introduction: Mesenchymal stem cells (MSCs) are multipotent progenitor cells that can differentiate in to osteoblast, adipocytes and chondrocytes. Lineage specification of MSC is governed by various systemic hormones, systemic and local growth factors and cytokines. TNF-α is an inflammatory cytokine produced at the site of tissue injuries and known to regulates MSC migration and differentiation. However, its role on lineage specification and differentiation of MSCs remain complex and elusive. In this study we explored the same utilizing human bone marrow and adipocyte derived MSCs. Experimental Methods: Human MSCs derived from bone marrow and adipocytes were differentiated in to osteoblast and adipocytes in the presence or absence of TNF-α. Expressions of osteoblast and adipocyte differentiation markers were assessed by qRT-PCR. The key epigenetic factor of lineage specification JMJD3 was depleted in MSCs utilizing lentiviral ShRNA. Results: TNF-α promoted the osteoblastic and inhibited the adipogenic differentiation of MSC as assessed by Alizarin and oil red O staining, respectively. Consistently, while inducing the key osteogenic factors, TNF- α repressed the adipogenic markers in MSCs. Mechanistically, TNF-α regulates MSC fate by inducing lysine-specific demethylase JMJD3/KDM6B, which is a key epigenetic factor that determines mesenchymal stem cell lineage specification. ShRNA mediated knockdown of JMD3 in MSCs inhibited TNF- α mediated activation and inhibition of osteogenic and adipogenic differentiation, respectively. Conclusion: Our study uncovers the novel mechanisms of TNF-α mediated MSC lineage commitment and differentiation and thus highlight JMJD3 as mediator of TNF-α actions in MSCs.
45
Lee, Meng-Jung, Heng Lin, Chi-Wei Liu, Min-Hua Wu, Wei-Ju Liao, Hsin-Huei Chang, Hui-Chen Ku, Yeh-Sheng Chien, Wang-Hsien Ding, and Yung-Hsi Kao. "Octylphenol stimulates resistin gene expression in 3T3-L1 adipocytes via the estrogen receptor and extracellular signal-regulated kinase pathways." American Journal of Physiology-Cell Physiology 294, no. 6 (June 2008): C1542—C1551. http://dx.doi.org/10.1152/ajpcell.00403.2007.
Full textAbstract:
Resistin is known as an adipocyte-specific secretory hormone that can cause insulin resistance and decrease adipocyte differentiation. It can be regulated by sexual hormones. Whether environmental estrogens regulate the production of resistin is still not clear. Using 3T3-L1 adipocytes, we found that octylphenol upregulated resistin mRNA expression in dose- and time-dependent manners. The concentration of octylphenol that increased resistin mRNA levels by 50% was ∼100 nM within 6 h of treatment. The basal half-life of resistin mRNA induced by actinomycin D was lengthened by octylphenol treatment, suggesting that octylphenol decreases the rate of resistin mRNA degradation. In addition, octylphenol stimulated resistin protein expression and release. The basal half-life of resistin protein induced by cycloheximide was lengthened by octylphenol treatment, suggesting that octylphenol decreases the rate of resistin protein degradation. While octylphenol was shown to increase activities of the estrogen receptor (ER) and MEK1, signaling was demonstrated to be blocked by pretreatment with either ICI-182780 (an ERα antagonist) or U-0126 (a MEK1 inhibitor), in which both inhibitors prevented octylphenol-stimulated phosphorylation of ERK. These results imply that ERα and ERK are necessary for the octylphenol stimulation of resistin mRNA expression. Moreover, U-0126 antagonized the octylphenol-increased resistin protein expression and release. These data suggest that the way octylphenol signaling increases resistin protein levels is similar to that by which it increases resistin mRNA levels; it is likely mediated through an ERK-dependent pathway. In vivo, octylphenol increased adipose resistin mRNA expression and serum resistin and glucose levels, supporting its in vitro effect.
46
Ding, S. T., E. O. Smith, R. L. McNeel, and H. J. Mersmann. "Modulation of porcine adipocyte beta-adrenergic receptors by hormones and butyrate." Journal of Animal Science 78, no. 4 (2000): 927. http://dx.doi.org/10.2527/2000.784927x.
Full text
47
Chandra, Prakash, Sukhdeep S. Basra, Tai C. Chen, and Vin Tangpricha. "Alterations in Lipids and Adipocyte Hormones in Female-to-Male Transsexuals." International Journal of Endocrinology 2010 (2010): 1–4. http://dx.doi.org/10.1155/2010/945053.
Full textAbstract:
Testosterone therapy in men and women results in decreased high-density lipoprotein cholesterol (HDL) and increased low-density lipoprotein cholesterol (LDL). We sought to determine whether testosterone therapy has this same effect on lipid parameters and adipocyte hormones in female-to-male (FTM) transsexuals. Twelve FTM transsexuals provided a fasting lipid profile including serum total cholesterol, HDL, LDL, and triglycerides prior to and after 1 year of testosterone therapy (testosterone enanthate or cypionate 50–125 mg IM every two weeks). Subjects experienced a significant decrease in mean serum HDL (52±11to40±7 mg/dL)(P<.001). The mean LDL(P=.316), triglyceride(P=.910), and total cholesterol(P=.769)levels remained unchanged. In a subset of subjects, we measured serum leptin levels which were reduced by 25% but did not reach statistical significance(P=.181)while resistin levels remained unchanged. We conclude that testosterone therapy in FTM transsexuals can promote an increased atherogenic lipid profile by lowering HDL and possibly reduce serum leptin levels. However, long-term studies are needed to determine whether decreases in HDL result in adverse cardiovascular outcomes.
48
Yaturu, Subhashini, Susan Prado, and Sidney R. Grimes. "Changes in adipocyte hormones leptin, resistin, and adiponectin in thyroid dysfunction." Journal of Cellular Biochemistry 93, no. 3 (October 15, 2004): 491–96. http://dx.doi.org/10.1002/jcb.20188.
Full text
49
Marette, A., and L. J. Bukowiecki. "Stimulation of glucose transport by insulin and norepinephrine in isolated rat brown adipocytes." American Journal of Physiology-Cell Physiology 257, no. 4 (October 1, 1989): C714—C721. http://dx.doi.org/10.1152/ajpcell.1989.257.4.c714.
Full textAbstract:
The effects of insulin and norepinephrine on glucose transport, glucose uptake, and cell respiration were investigated in isolated rat brown adipocytes. Glucose transport and uptake were determined using [U-14C]-D-glucose and 2-deoxy-[1,2-3H]-D-glucose, respectively. Brown adipocyte respiration was measured polarographically. Dose-response experiments revealed that insulin stimulated D-glucose transport and 2-deoxyglucose uptake between 10(-11) and 10(-7) M with a maximal four- to sixfold stimulation. In the absence of insulin, norepinephrine concentrations ranging from 10(-7) to 10(-7) M also enhanced glucose transport and uptake with a maximal two- to fourfold stimulation. Experiments with alpha- and beta-adrenergic agonists and antagonists showed that the effect of norepinephrine was predominantly mediated via beta-adrenergic pathways. Dibutyryl cyclic AMP and 3-isobutyl-1-methylxanthine also increased glucose transport, suggesting that the effects of norepinephrine are cyclic AMP dependent. Moreover, norepinephrine (10(-8) M) enhanced insulin sensitivity for glucose transport [half-maximum velocity constant (1/2 V max)] but failed to potentiate insulin responsiveness (Vmax). On the other hand, insulin (10(-9) M) had no effect on basal respiration but rapidly inhibited the calorigenic effect of norepinephrine (10(-7) M) by greater than 50%. These results demonstrate that 1) in the absence of insulin, physiological concentrations of norepinephrine stimulate glucose transport via beta-adrenergic pathways, 2) the neurohormone synergistically potentiates brown adipocyte submaximal insulin responses for glucose transport, and 3) insulin counteracts the effects of norepinephrine on brown adipocyte thermogenesis despite the fact that both hormones enhance glucose uptake.
50
Ciaraldi, T. P., R. Horuk, and S. Matthaei. "Biochemical and functional characterization of the rat liver glucose-transport system Comparisons with the adipocyte glucose-transport system." Biochemical Journal 240, no. 1 (November 15, 1986): 115–23. http://dx.doi.org/10.1042/bj2400115.
Full textAbstract:
The properties of the glucose-transport systems in rat adipocytes and hepatocytes were compared in cells prepared from the same animals. Hormones and other agents which cause a large stimulation of 3-O-methylglucose transport in adipocytes were without acute effect in hepatocytes. Hepatocytes displayed a lower affinity for 3-O-methylglucose (20 mM) and alternative substrates than adipocytes (6 mM), whereas inhibitor affinities were similar in both cell types. The concentration and distribution of glucose transporters were determined by Scatchard analysis of D-glucose-inhibitable [3H]cytochalasin B binding to subcellular fractions. In liver, most of the transporters were located in the plasma membrane (42 +/- 5 pmol/mg of protein) with a small amount (4 +/- 3 pmol/mg) in the low-density microsomal fraction (‘microsomes’), the reverse of the situation in adipocytes. Glucose transporters were covalently labelled with [3H]cytochalasin B by using the photochemical cross-linking agent hydroxysuccinimidyl-4-azidobenzoate and analysed by SDS/polyacrylamide-gel electrophoresis. A single D-glucose-inhibitable peak with a molecular mass of 40-50 kDa was seen in both plasma membrane and low-density microsomes. This peak was further characterized by isoelectric focusing and revealed a single peak of specific [3H]cytochalasin B binding at pI 6.05 in both low-density microsomes and plasma membrane, compared with peaks at pI 6.4 and 5.6 in adipocyte membranes. In summary: the glucose-transport system in hepatocytes has a lower affinity and higher capacity than that in adipocytes, and is also not accurately modulated by insulin; the subcellular distribution of glucose transporters in the liver suggests that few intracellular transporters would be available for translocation; the liver transporter has a molecular mass similar to that of the adipocyte transporter; the liver glucose transporter exists as a single charged form (pI 6.05), compared with the multiple forms in adipocytes. This difference in charge could reflect a functionally important difference in molecular structure between the two cell types.