Journal articles: 'Endocrine and paracrine regulations'

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Martin, Thomas John. "Endocrine and paracrine regulation of bone." Future Rheumatology 3, no. 2 (April 2008): 117–19. http://dx.doi.org/10.2217/17460816.3.2.117.

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TAYLOR, ROBERT N., DAN I. LEBOVIC, DANIELA HORNUNG, and MICHAEL D. MUELLER. "Endocrine and Paracrine Regulation of Endometrial Angiogenesis." Annals of the New York Academy of Sciences 943, no. 1 (September 2001): 109–21. http://dx.doi.org/10.1111/j.1749-6632.2001.tb03795.x.

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SAEZ, JOSÉ M. "Leydig Cells: Endocrine, Paracrine, and Autocrine Regulation." Endocrine Reviews 15, no. 5 (October 1994): 574–626. http://dx.doi.org/10.1210/edrv-15-5-574.

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Salustri, Antonietta, Antonella Camaioni, and Cristina D'Alessandris. "Endocrine and paracrine regulation of cumulus expansion." Zygote 4, no. 04 (November 1996): 313–15. http://dx.doi.org/10.1017/s0967199400003312.

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In a Graafian follicle, granulosa cells are classified into two principal cell subpopulations: cumulus cells, which are closely associated with the oocyte to form the cumulus cell-oocyte complex (COC), and mural granulosa cells, which are organised as a stratified epithelium at the periphery of the follicle. Following the preovulatory gonadotropin surge, cumulus cells lose contact with mural granulosa cells and start to synthesise and secrete a large amount of hyaluronan (HA), a glycosaminoglycan with high molecular weight and large hydrodynamic domains (Salustriet al., 1992). Proteins derived from serum (Chenet al., 1992, 1994) and synthesised by cumulus cells (Camaioniet al., 1993, 1996) organise the strands of HA into an intercellular elastic network that traps the cumulus cells and the oocyte in a unit which can not be mechanically dissociated – a process also referred to as cumulus expansion. At ovulation, the expanded COC is released through the ruptured follicle wall and transferred to the oviduct. The matrix in the expanded COC facilitates its extrusion from the follicle and its capture by oviductal fimbria, and provides, together with the cumulus cells, a suitable microenvironment for sperm penetration and fertilisation (for references see Salustriet al., 1993).

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Sims, Natalie A., and Ling Yeong Chia. "Regulation of Sclerostin Expression by Paracrine and Endocrine Factors." Clinical Reviews in Bone and Mineral Metabolism 10, no. 2 (November 16, 2011): 98–107. http://dx.doi.org/10.1007/s12018-011-9121-7.

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Carbillon, Lionel, Michele Uzan, Jean-Claude Challier, Philippe Merviel, and Serge Uzan. "Fetal-Placental and Decidual-Placental Units: Role of Endocrine and Paracrine Regulations in Parturition." Fetal Diagnosis and Therapy 15, no. 5 (2000): 308–18. http://dx.doi.org/10.1159/000021027.

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Biswas, Subhasri, Urmi Mukherjee, and Sudipta Maitra. "Endocrine disruption and female reproductive health: Implications on cross-talk between endocrine and autocrine/paracrine axes in the ovary." Journal of Reproductive Health and Medicine 3 (November 10, 2020): 2. http://dx.doi.org/10.25259/jrhm_11_2020.

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Female reproduction is a blend of neuroendocrine, endocrine, and autocrine/paracrine factors that maintain the appropriate ovarian micro-environment. The growing urbanization prompted exposure to a myriad of environmental toxins carrying the ability to interfere with reproductive processes governed by endogenous hormones, making reproductive health a major global concern. These environmental anthropogenic contaminants, popularly termed as endocrine-disrupting chemicals (EDCs), can disrupt the ovarian homeostasis leading to serious perturbations, namely, anovulation, infertility, estrogen deficiency, and premature ovarian failure. Although gonadotropin action, biosynthesis of gonadal steroids vis-à-vis growth factors comprise the essential modulators within the ovary, the redox balance along with inflammatory and cell death response can dramatically influence the framework of ovarian dynamics; however, details of which remain relatively less understood. The present overview provides an update on candidates (endocrines and autocrine/paracrine) of oogenesis, and the potential impact of EDCs on diverse intra-ovarian entities including but not limited to gonadotropin action, steroidogenic potential, expression of growth factors, and modulation of maturational competence. Moreover, the relative importance of free radical-induced stress, inflammation, and elevated cell death (follicular atresia), in the regulation of ovarian functions and how these intricate yet conjoined mechanisms may alter the reproductive performance of a female will be an issue of discussion.

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Polidoro, Juliano Z., Weverton M. Luchi, Antonio Carlos Seguro, Gerhard Malnic, and Adriana C. C. Girardi. "Paracrine and endocrine regulation of renal K⁺ secretion." American Journal of Physiology-Renal Physiology 322, no. 3 (March 1, 2022): F360—F377. http://dx.doi.org/10.1152/ajprenal.00251.2021.

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The seminal studies conducted by Giebisch and coworkers in the 1960s paved the way for understanding the renal mechanisms involved in K+ homeostasis. It was demonstrated that differential handling of K+ in the distal segments of the nephron is crucial for proper K+ balance. Although aldosterone had been classically ascribed as the major ion transport regulator in the distal nephron, thereby contributing to K+ homeostasis, it became clear that aldosterone per se could not explain the ability of the kidney to modulate kaliuresis in both acute and chronic settings. The existence of alternative kaliuretic and antikaliuretic mechanisms was suggested by physiological studies in the 1980s but only gained form and shape with the advent of molecular biology. It is now established that the kidneys recruit several endocrine and paracrine mechanisms for adequate kaliuretic response. These mechanisms include the direct effects of peritubular K+, a gut-kidney regulatory axis sensing dietary K+ levels, the kidney secretion of kallikrein during postprandial periods, the upregulation of angiotensin II receptors in the distal nephron during chronic changes in K+ diet, and the local increase of prostaglandins by low-K+ diet. This review discusses recent advances in the understanding of endocrine and paracrine mechanisms underlying the modulation of K+ secretion and how these mechanisms impact kaliuresis and K+ balance. We also highlight important unknowns about the regulation of renal K+ excretion under physiological circumstances.

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Challis, J. R. G. "Endocrine and Paracrine Regulation of Birth at Term and Preterm." Endocrine Reviews 21, no. 5 (October 1, 2000): 514–50. http://dx.doi.org/10.1210/er.21.5.514.

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Challis, John R. G., Stephen G. Matthews, William Gibb, and Stephen J. Lye. "Endocrine and Paracrine Regulation of Birth at Term and Preterm*." Endocrine Reviews 21, no. 5 (October 1, 2000): 514–50. http://dx.doi.org/10.1210/edrv.21.5.0407.

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Abstract We have examined factors concerned with the maintenance of uterine quiescence during pregnancy and the onset of uterine activity at term in an animal model, the sheep, and in primate species. We suggest that in both species the fetus exerts a critical role in the processes leading to birth, and that activation of the fetal hypothalamic-pituitary-adrenal axis is a central mechanism by which the fetal influence on gestation length is exerted. Increased cortisol output from the fetal adrenal gland is a common characteristic across animal species. In primates, there is, in addition, increased output of estrogen precursor from the adrenal in late gestation. The end result, however, in primates and in sheep is similar: an increase in estrogen production from the placenta and intrauterine tissues. We have revised the pathway by which endocrine events associated with parturition in the sheep come about and suggest that fetal cortisol directly affects placental PGHS expression. In human pregnancy we suggest that cortisol increases PGHS expression, activity, and PG output in human fetal membranes in a similar manner. Simultaneously, cortisol contributes to decreases in PG metabolism and to a feed-forward loop involving elevation of CRH production from intrauterine tissues. In human pregnancy, there is no systemic withdrawal of progesterone in late gestation. We have argued that high circulating progesterone concentrations are required to effect regionalization of uterine activity, with predominantly relaxation in the lower uterine segment, allowing contractions in the fundal region to precipitate delivery. This new information, arising from basic and clinical studies, should further the development of new methods of diagnosing the patient at risk of preterm labor, and the use of scientifically based strategies specifically for the management of this condition, which will improve the health of the newborn.

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Jabbour, Henry N., Rodney W. Kelly, Hamish M. Fraser, and Hilary O. D. Critchley. "Endocrine Regulation of Menstruation." Endocrine Reviews 27, no. 1 (September 13, 2005): 17–46. http://dx.doi.org/10.1210/er.2004-0021.

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In women, endometrial morphology and function undergo characteristic changes every menstrual cycle. These changes are crucial for perpetuation of the species and are orchestrated to prepare the endometrium for implantation of a conceptus. In the absence of pregnancy, the human endometrium is sloughed off at menstruation over a period of a few days. Tissue repair, growth, angiogenesis, differentiation, and receptivity ensue to prepare the endometrium for implantation in the next cycle. Ovarian sex steroids through interaction with different cognate nuclear receptors regulate the expression of a cascade of local factors within the endometrium that act in an autocrine/paracrine and even intracrine manner. Such interactions initiate complex events within the endometrium that are crucial for implantation and, in the absence thereof, normal menstruation. A clearer understanding of regulation of normal endometrial function will provide an insight into causes of menstrual dysfunction such as menorrhagia (heavy menstrual bleeding) and dysmenorrhea (painful periods). The molecular pathways that precipitate these pathologies remain largely undefined. Future research efforts to provide greater insight into these pathways will lead to the development of novel drugs that would target identified aberrations in expression and/or of local uterine factors that are crucial for normal endometrial function.

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Kumar, A., S. Raut, and N. H. Balasinor. "Endocrine regulation of sperm release." Reproduction, Fertility and Development 30, no. 12 (2018): 1595. http://dx.doi.org/10.1071/rd18057.

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Spermiation (sperm release) is the culmination of a spermatid’s journey in the seminiferous epithelium. After a long association with the Sertoli cell, spermatids have to finally ‘let go’ of the support from Sertoli cells in order to be transported to the epididymis. Spermiation is a multistep process characterised by removal of excess spermatid cytoplasm, recycling of junctional adhesion molecules by endocytosis, extensive cytoskeletal remodelling and final spermatid disengagement. Successful execution of all these events requires coordinated regulation by endocrine and paracrine factors. This review focuses on the endocrine regulation of spermiation. With the aim of delineating how hormones control the various aspects of spermiation, this review provides an analysis of recent advances in research on the hormonal control of molecules associated with the spermiation machinery. Because spermiation is one of the most sensitive phases of spermatogenesis to variations in hormone levels, understanding their molecular control is imperative to advance our knowledge of the nuances of spermatogenesis and male fertility.

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Birzniece, Vita, and Ken K. Y. Ho. "MECHANISMS IN ENDOCRINOLOGY: Paracrine and endocrine control of the growth hormone axis by estrogen." European Journal of Endocrinology 184, no. 6 (June 1, 2021): R269—R278. http://dx.doi.org/10.1530/eje-21-0155.

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There is a strong biological link between the growth hormone (GH) and gonadal systems in growth, development and metabolism; however, regulatory interactions are poorly understood. Advances in estrogen biology and endocrine physiology have provided insights into mechanistic links between the two systems. Estrogens are synthesized from androgens by aromatase which is widely distributed in extragonadal tissues. Local generation of estrogens raise the possibility of paracrine control as an additional level to classical endocrine regulation of the GH system. To explore the mechanistic links, we review the pharmacology of estrogen, the effects of estrogen replacement, antagonism, and the impact of aromatase inhibition on the GH system as well as the metabolic sequelae. In men, estrogens derived from androgens drive the central secretion of GH, independent of the androgen receptor. In hypogonadal women, physiological replacement via a parenteral route evokes no effect while estrogen receptor antagonism and estrogen deprivation induce disparate effects, providing no consistent evidence that estrogens regulate the central secretion of GH via paracrine or endocrine mechanisms. However, delivery of estrogen by the oral route inhibits hepatic IGF-1 production, in turn increasing GH secretion via reduced feedback inhibition. This endocrine route-dependent effect of oral estrogen compounds on hepatic function induces detrimental metabolic effects on hypogonadal women. In conclusion, estrogens regulate the secretion and action of GH via complex paracrine and endocrine interactions and impart metabolic effects in a route- and gender-dependent manner. The metabolic sequelae of compounds mimicking, antagonizing, or depleting estrogens, should be considered in tailoring and optimizing their use.

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Heindel, Jerrold J., and Kimberley A. Treinen. "Physiology of the Male Reproductive System: Endocrine, Paracrine and Autocrine Regulation." Toxicologic Pathology 17, no. 2 (February 1989): 411–45. http://dx.doi.org/10.1177/019262338901700219.

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Hill, Thomas G., and David J. Hill. "The Importance of Intra-Islet Communication in the Function and Plasticity of the Islets of Langerhans during Health and Diabetes." International Journal of Molecular Sciences 25, no. 7 (April 6, 2024): 4070. http://dx.doi.org/10.3390/ijms25074070.

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Islets of Langerhans are anatomically dispersed within the pancreas and exhibit regulatory coordination between islets in response to nutritional and inflammatory stimuli. However, within individual islets, there is also multi-faceted coordination of function between individual beta-cells, and between beta-cells and other endocrine and vascular cell types. This is mediated partly through circulatory feedback of the major secreted hormones, insulin and glucagon, but also by autocrine and paracrine actions within the islet by a range of other secreted products, including somatostatin, urocortin 3, serotonin, glucagon-like peptide-1, acetylcholine, and ghrelin. Their availability can be modulated within the islet by pericyte-mediated regulation of microvascular blood flow. Within the islet, both endocrine progenitor cells and the ability of endocrine cells to trans-differentiate between phenotypes can alter endocrine cell mass to adapt to changed metabolic circumstances, regulated by the within-islet trophic environment. Optimal islet function is precariously balanced due to the high metabolic rate required by beta-cells to synthesize and secrete insulin, and they are susceptible to oxidative and endoplasmic reticular stress in the face of high metabolic demand. Resulting changes in paracrine dynamics within the islets can contribute to the emergence of Types 1, 2 and gestational diabetes.

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Shinoda, Yusuke, Masayuki Yamaguchi, Naoshi Ogata, Toru Akune, Naoto Kubota, Toshimasa Yamauchi, Yasuo Terauchi, et al. "Regulation of bone formation by adiponectin through autocrine/paracrine and endocrine pathways." Journal of Cellular Biochemistry 99, no. 1 (2006): 196–208. http://dx.doi.org/10.1002/jcb.20890.

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Salamonsen, LA, and JK Findlay. "Regulation of endometrial prostaglandins during the menstrual cycle and in early pregnancy." Reproduction, Fertility and Development 2, no. 5 (1990): 443. http://dx.doi.org/10.1071/rd9900443.

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Prostaglandins are important regulators of endometrial function. In turn, their secretion is controlled by endocrine and paracrine mediators. Cyclical effects of ovarian oestrogen and progesterone throughout the menstrual or oestrous cycle result in overall higher levels of prostaglandin release during the secretory or luteal phase of the cycle than during the proliferative phase. Potential paracrine regulators of endometrial origin include cytokines, growth factors and histamine, some of which may arise from infiltrating cells. Embryo-derived factors can regulate endometrial prostaglandin release in early pregnancy. Both platelet-activating factor and ovine trophoblast protein-1 (an embryonic interferon) modify prostaglandin release from primary cultures of endometrial cells of human and ovine origin respectively. Manipulation of such mediators may provide new means for fertility control.

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Kniss, Douglas A., and Jay D. Iams. "Regulation of Parturition Update: Endocrine and Paracrine Effectors of Term and Preterm Labor." Clinics in Perinatology 25, no. 4 (December 1998): 819–36. http://dx.doi.org/10.1016/s0095-5108(18)30085-x.

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SHUBHADA, SANKARARAMAN, MAURUS GLINZ, and DOLORES J. LAMB. "Sertoli Cell Secreted Growth Factor Cellular Origin, Paracrine and Endocrine Regulation of Secretion." Journal of Andrology 14, no. 2 (March 4, 1993): 99–109. http://dx.doi.org/10.1002/j.1939-4640.1993.tb01659.x.

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ABSTRACT: Rat and human Sertoli cells in culture secrete a growth factor, Serfoli cell secreted growth factor (SCSGF). The aims of the present study were (1) to evaluate other testicular cell types as additional sources of SCSGF, as well as their paracrine effect, and (2) to study the hormonal regulation of SCSGF secretion using an A431 cell growth assay. The Sertoli cell was the only testicular cell type tested that secreted SCSGF activity in vitro. Peritubular cells enhanced Sertoli cell attachment and SCSGF secretion. Spermatogenic cells had no effect. The secretion of SCSGF was specifically stimulated by follicle‐stimulating hormone (FSH) and testosterone. Treatment with agents that increase intracellular cAMP levels and adenosine stimulated the secretion of mitogenic activity into Sertoli cell‐conditioned medium by three‐ to fivefold. This growth factor, secreted by the Sertoli cell and regulated by FSH and testosterone, may play a critical role in the regulation of spermatogenesis.

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Schumacher, Justin D., and Grace L. Guo. "Regulation of Hepatic Stellate Cells and Fibrogenesis by Fibroblast Growth Factors." BioMed Research International 2016 (2016): 1–8. http://dx.doi.org/10.1155/2016/8323747.

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Fibroblast growth factors (FGFs) are a family of growth factors critically involved in developmental, physiological, and pathological processes, including embryogenesis, angiogenesis, wound healing, and endocrine functions. In the liver, several FGFs are produced basally by hepatocytes and hepatic stellate cells (HSCs). Upon insult to the liver, expression of FGFs in HSCs is greatly upregulated, stimulating hepatocyte regeneration and growth. Various FGF isoforms have also been shown to directly induce HSC proliferation and activation thereby enabling autocrine and paracrine regulation of HSC function. Regulation of HSCs by the endocrine FGFs, namely, FGF15/19 and FGF21, has also recently been identified. With the ability to modulate HSC proliferation and transdifferentiation, targeting FGF signaling pathways constitutes a promising new therapeutic strategy to treat hepatic fibrosis.

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Lavoie, Julie L., and Curt D. Sigmund. "Minireview: Overview of the Renin-Angiotensin System—An Endocrine and Paracrine System." Endocrinology 144, no. 6 (June 1, 2003): 2179–83. http://dx.doi.org/10.1210/en.2003-0150.

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Abstract Since the discovery of renin as a pressor substance in 1898, the renin-angiotensin (RAS) system has been extensively studied because it remains a prime candidate as a causative factor in the development and maintenance of hypertension. Indeed, some of the properties of the physiologically active component of the RAS, angiotensin II, include vasoconstriction, regulation of renal sodium and water absorption, and increasing thirst. Initially, its affect on blood pressure was thought to be mediated primarily through the classical endocrine pathway; that is, the generation of blood-borne angiotensin with actions in target tissues. More recently, however, it has become appreciated that a local autocrine or paracrine RAS may exist in a number of tissues, and that these may also play a significant role in regulating blood pressure. Some of the difficulties in studying tissue RAS stem from the limitations of pharmacology in not differentiating between RAS products made systemically from those synthesized locally. However, the development of transgenic animals with highly specific promoters to target the RAS to specific tissues provided important tools to dissect these systems. Thus, this minireview will discuss recent advances in understanding the relationship between endocrine and paracrine (tissue) RAS using transgenic models.

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Ruginsk, Silvia Graciela, Andre de Souza Mecawi, Melina Pires da Silva, Wagner Luis Reis, Ricardo Coletti, Juliana Bezerra Medeiros de Lima, Lucila Leico Kagohara Elias, and Jose Antunes-Rodrigues. "Gaseous Modulators in the Control of the Hypothalamic Neurohypophyseal System." Physiology 30, no. 2 (March 2015): 127–38. http://dx.doi.org/10.1152/physiol.00040.2014.

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Nitric oxide (NO), carbon monoxide (CO), and hydrogen sulfide (H2S) are gaseous molecules produced by the brain. Within the hypothalamus, gaseous molecules have been highlighted as autocrine and paracrine factors regulating endocrine function. Therefore, in the present review, we briefly discuss the main findings linking NO, CO, and H2S to the control of body fluid homeostasis at the hypothalamic level, with particular emphasis on the regulation of neurohypophyseal system output.

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Moede, Tilo, Ingo B. Leibiger, and Per-Olof Berggren. "Alpha cell regulation of beta cell function." Diabetologia 63, no. 10 (September 7, 2020): 2064–75. http://dx.doi.org/10.1007/s00125-020-05196-3.

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Abstract The islet of Langerhans is a complex endocrine micro-organ consisting of a multitude of endocrine and non-endocrine cell types. The two most abundant and prominent endocrine cell types, the beta and the alpha cells, are essential for the maintenance of blood glucose homeostasis. While the beta cell produces insulin, the only blood glucose-lowering hormone of the body, the alpha cell releases glucagon, which elevates blood glucose. Under physiological conditions, these two cell types affect each other in a paracrine manner. While the release products of the beta cell inhibit alpha cell function, the alpha cell releases factors that are stimulatory for beta cell function and increase glucose-stimulated insulin secretion. The aim of this review is to provide a comprehensive overview of recent research into the regulation of beta cell function by alpha cells, focusing on the effect of alpha cell-secreted factors, such as glucagon and acetylcholine. The consequences of differences in islet architecture between species on the interplay between alpha and beta cells is also discussed. Finally, we give a perspective on the possibility of using an in vivo imaging approach to study the interactions between human alpha and beta cells under in vivo conditions.

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Kjekshus, Harald, Otto A. Smiseth, Randi Klinge, Erik Øie, Marit E. Hystad, and Håvard Attramadal. "Regulation of ET: pulmonary release of ET contributes to increased plasma ET levels and vasoconstriction in CHF." American Journal of Physiology-Heart and Circulatory Physiology 278, no. 4 (April 1, 2000): H1299—H1310. http://dx.doi.org/10.1152/ajpheart.2000.278.4.h1299.

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Endothelin (ET) contributes to the increased systemic vascular resistance and elevated cardiac filling pressures seen in congestive heart failure (CHF). We investigated to what extent ET-mediated vasoconstriction in CHF occurs through an endocrine action of elevated plasma ET or by an autocrine/paracrine mechanism related to induction of vascular ET gene expression. Three weeks of pacing (225 beats/min) induced a marked release of ET-1 from the pulmonary circulation with a sixfold elevation of arterial plasma ET in CHF pigs compared with sham-operated pigs. Arterial plasma ET was the strongest and only independent predictor of systemic vascular resistance. In contrast, vascular preproET-1 and ET-receptor mRNA expression were unaltered or decreased in CHF pigs and did not correlate with indexes of vascular tone. However, myocardial preproET-1 mRNA expression increased twofold in CHF pigs. PreproET-2 and preproET-3 mRNAs were not detectable in cardiovascular tissues. In conclusion, plasma ET was markedly increased because of an augmented release from the pulmonary circulation during CHF, and arterial plasma ET correlated with systemic vascular resistance. The absence of ET induction in the peripheral vasculature suggests that ET increases vascular tone during CHF by an endocrine, not an autocrine/paracrine, mechanism.

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Gao, Rui, Tao Yang, and Quan Zhang. "δ-Cells: The Neighborhood Watch in the Islet Community." Biology 10, no. 2 (January 21, 2021): 74. http://dx.doi.org/10.3390/biology10020074.

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Somatostatin-secreting δ-cells have aroused great attention due to their powerful roles in coordination of islet insulin and glucagon secretion and maintenance of glucose homeostasis. δ-cells exhibit neuron-like morphology with projections which enable pan-islet somatostatin paracrine regulation despite their scarcity in the islets. The expression of a range of hormone and neurotransmitter receptors allows δ-cells to integrate paracrine, endocrine, neural and nutritional inputs, and provide rapid and precise feedback modulations on glucagon and insulin secretion from α- and β-cells, respectively. Interestingly, the paracrine tone of δ-cells can be effectively modified in response to factors released by neighboring cells in this interactive communication, such as insulin, urocortin 3 and γ-aminobutyric acid from β-cells, glucagon, glutamate and glucagon-like peptide-1 from α-cells. In the setting of diabetes, defects in δ-cell function lead to suboptimal insulin and glucagon outputs and lift the glycemic set-point. The interaction of δ-cells and non-δ-cells also becomes defective in diabetes, with reduces paracrine feedback to β-cells to exacerbate hyperglycemia or enhanced inhibition of α-cells, disabling counter-regulation, to cause hypoglycemia. Thus, it is possible to restore/optimize islet function in diabetes targeting somatostatin signaling, which could open novel avenues for the development of effective diabetic treatments.

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Arkprabha, Naik, Sreelakshmi Namburu, and Veereshbabu Prathap. "The Science of Pigmentation: Melanin Synthesis and Regulation." Journal of Pharmacological Research and Developments 6, no. 2 (November 7, 2024): 1–10. http://dx.doi.org/10.46610/jprd.2024.v06i02.001.

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Melanin, the primary pigment that defines skin color, is also crucial for protecting the skin from U.V. radiation damage. Melanin production, or melanogenesis, is an intricate biochemical process involving several enzymes, hormones, and metal ions. Adrenocorticotropic hormone (ACTH) and melanocortin (MSH) are essential hormones that regulate melanogenesis through endocrine, autocrine, and paracrine processes. Exposure to U.V. radiation stimulates the release of these hormones, leading to increased melanin production and skin pigmentation. The presence of different metal ions during the melanogenesis process can also affect the structure and properties of the final melanin pigment.

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Phan, Phuc, Bibhuti Ballav Saikia, Shivakumar Sonnaila, Shilpi Agrawal, Zeina Alraawi, Thallapuranam Krishnaswamy Suresh Kumar, and Shilpa Iyer. "The Saga of Endocrine FGFs." Cells 10, no. 9 (September 14, 2021): 2418. http://dx.doi.org/10.3390/cells10092418.

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Fibroblast growth factors (FGFs) are cell-signaling proteins with diverse functions in cell development, repair, and metabolism. The human FGF family consists of 22 structurally related members, which can be classified into three separate groups based on their action of mechanisms, namely: intracrine, paracrine/autocrine, and endocrine FGF subfamilies. FGF19, FGF21, and FGF23 belong to the hormone-like/endocrine FGF subfamily. These endocrine FGFs are mainly associated with the regulation of cell metabolic activities such as homeostasis of lipids, glucose, energy, bile acids, and minerals (phosphate/active vitamin D). Endocrine FGFs function through a unique protein family called klotho. Two members of this family, α-klotho, or β-klotho, act as main cofactors which can scaffold to tether FGF19/21/23 to their receptor(s) (FGFRs) to form an active complex. There are ongoing studies pertaining to the structure and mechanism of these individual ternary complexes. These studies aim to provide potential insights into the physiological and pathophysiological roles and therapeutic strategies for metabolic diseases. Herein, we provide a comprehensive review of the history, structure–function relationship(s), downstream signaling, physiological roles, and future perspectives on endocrine FGFs.

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Jaworski, Kathy, Eszter Sarkadi-Nagy, Robin E. Duncan, Maryam Ahmadian, and Hei Sook Sul. "Regulation of Triglyceride Metabolism.IV. Hormonal regulation of lipolysis in adipose tissue." American Journal of Physiology-Gastrointestinal and Liver Physiology 293, no. 1 (July 2007): G1—G4. http://dx.doi.org/10.1152/ajpgi.00554.2006.

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Triacylglycerol (TAG) stored in adipose tissue can be rapidly mobilized by the hydrolytic action of lipases, with the release of fatty acids (FA) that are used by other tissues during times of energy deprivation. Unlike synthesis of TAG, which occurs not only in adipose tissue but also in other tissues such as liver for very-low-density lipoprotein formation, hydrolysis of TAG, lipolysis, predominantly occurs in adipose tissue. Until recently, hormone-sensitive lipase was considered to be the key rate-limiting enzyme responsible for regulating TAG mobilization. However, recent studies on hormone-sensitive lipase-null mice have challenged such a concept. A novel lipase named desnutrin/ATGL has been recently discovered to play a key role in lipolysis in adipocytes. Lipolysis is under tight hormonal regulation. Although opposing regulation of lipolysis in adipose tissue by insulin and catecholamines is well understood, autocrine/paracrine factors may also participate in its regulation. Intricate cooperation of these endocrine and autocrine/paracrine factors leads to a fine regulation of lipolysis in adipocytes, needed for energy homeostasis. In this review, we summarize and discuss the recent progress made in the regulation of adipocyte lipolysis.

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Rahbi, Hazim, Hafid Narayan, Donald J. L. Jones, and Leong L. Ng. "The uroguanylin system and human disease." Clinical Science 123, no. 12 (August 10, 2012): 659–68. http://dx.doi.org/10.1042/cs20120021.

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The uroguanylin system is a newly discovered endocrine/paracrine system that may have a role in the regulation of salt balance, appetite and gut health. The precursor pro-uroguanylin is predominantly synthesized in the gut, although there may be other sites of synthesis, including the kidney tubules. Products from pro-uroguanylin may mediate natriuresis following oral consumption of a salt load through both GC-C (guanylate cyclase C)-dependent and -independent mechanisms, and recent evidence suggests a role in appetite regulation. Local paracrine effects in the gut through GC-C stimulation may have tumour-suppressing actions through the regulation of cell proliferation and metabolism. Although most information on this system has been derived from knockout models, recent human studies have indicated possible roles in heart failure and renal failure. An improved understanding of the nature of its natriuretic, appetite and tumour-suppressing actions may facilitate the discovery of new therapies for heart failure, obesity and cancer prophylaxis.

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Bossé, Ynuk. "Endocrine regulation of airway contractility is overlooked." Journal of Endocrinology 222, no. 2 (June 13, 2014): R61—R73. http://dx.doi.org/10.1530/joe-14-0220.

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Asthma is a prevalent respiratory disorder triggered by a variety of inhaled environmental factors, such as allergens, viruses, and pollutants. Asthma is characterized by an elevated activation of the smooth muscle surrounding the airways, as well as a propensity of the airways to narrow excessively in response to a spasmogen (i.e. contractile agonist), a feature called airway hyperresponsiveness. The level of airway smooth muscle (ASM) activation is putatively controlled by mediators released in its vicinity. In asthma, many mediators that affect ASM contractility originate from inflammatory cells that are mobilized into the airways, such as eosinophils. However, mounting evidence indicates that mediators released by remote organs can also influence the level of activation of ASM, as well as its level of responsiveness to spasmogens and relaxant agonists. These remote mediators are transported through circulating blood to act either directly on ASM or indirectly via the nervous system by tuning the level of cholinergic activation of ASM. Indeed, mediators generated from diverse organs, including the adrenals, pancreas, adipose tissue, gonads, heart, intestines, and stomach, affect the contractility of ASM. Together, these results suggest that, apart from a paracrine mode of regulation, ASM is subjected to an endocrine mode of regulation. The results also imply that defects in organs other than the lungs can contribute to asthma symptoms and severity. In this review, I suggest that the endocrine mode of regulation of ASM contractility is overlooked.

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Liu, Xiaoqiang, Pengyun Qiao, Aifang Jiang, Junyi Jiang, Haiyan Han, Li Wang, and Chune Ren. "Paracrine Regulation of Steroidogenesis in Theca Cells by Granulosa Cells Derived from Mouse Preantral Follicles." BioMed Research International 2015 (2015): 1–8. http://dx.doi.org/10.1155/2015/925691.

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Interaction partners of follicular cells play a significant role in steroidogenesis, follicular formation, and development. Androgen secreted by theca cells (TCs) can initiate follicle development and ovulation and provide precursor materials for estrogen synthesis. Therefore, studies on ovarian microenvironment will not only lead to better understanding of the steroidogenesis but also have clinical significance for ovarian endocrine abnormalities such as hyperandrogenism in polycystic ovary syndrome (PCOS). This study applied the Transwell coculture model to investigate if the interaction between granulosa and theca cells may affect androgen production in theca cells. Concentrations of testosterone and androstenedione in the spent medium were measured by radioimmunoassay and enzyme linked immunosorbent assay, respectively. The results show that the coculture with granulosa cells (GCs) increases steroidogenesis in TCs. In addition, testosterone and androstenedione productions in response to LH stimulation were also increased in the coculture model. Significantly increased mRNA expressions of steroidogenic enzymes (Star,Cyp11a1,Cyp17a1, andHsd3b2) were observed in the cocultured TCs. Thus, GCs were capable of promoting steroidogenesis and LH responsiveness in TCs. This study provided a basis for further exploration of ovarian endocrine mechanism and pathologies.

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Renner, Ulrich, Uberto Pagotto, Eduardo Arzt, and Günter Karl Stalla. "Autocrine and paracrine roles of polypeptide growth factors, cytokines and vasogenic substances in normal and tumorous pituitary function and growth: a review." European Journal of Endocrinology 135, no. 5 (November 1996): 515–32. http://dx.doi.org/10.1530/eje.0.1350515.

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Renner U, Pagotto U, Arzt E, Stalla GK. Autocrine and paracrine roles of polypeptide growth factors, cytokines and vasogenic substances in normal and tumorous pituitary function and growth: a review. Eur J Endocrinol 1996;135:515–32. ISSN 0804–4643 In addition to the classical hormones, the production of numerous polypeptide growth factors, cytokines, vasogenic substances and neuropeptides by pituitary cells has been demonstrated. Expression of the corresponding receptors on pituitary cells enables these factors to influence growth and function of the pituitary by auto- or paracrine mechanisms. Thus, in addition to the external endocrine control of pituitary growth and function, an intrinsic intercellular communication network seems to be involved in the control of pituitary homeostasis. The cell-to-cell communication may be of importance for the pre- and postnatal differentiation of the pituitary, for the regulation of the cellular composition of the gland (by balancing mitosis and apoptosis and controlling angiogenesis) and for the adaption of pituitary function to altered physiological conditions (i.e. stress, pregnancy and diseases). Differences in the expression of or the response to the above-mentioned factors in pituitary adenomas indicate that these substances are of importance for pituitary tumorigenesis. Disturbances of auto-/paracrine mechanisms may not necessarily be involved in the tumor initiation processes, but they may play a crucial role in tumor progression. After the initial transformation, the clonal expansion of the tumor cell is dependent on its ability to escape either from the inhibitory action of growth suppressing factors or to develop an autocrine mechanism that allows autonomous growth. In summary, therefore, this review outlines the potential role of polypeptide growth factors, cytokines and vasogenic peptides as auto-/paracrine-acting substances in normal pituitary and pituitary adenomas. Ulrich Renner, Max-Planck-Institute of Psychiatry, Clinical Institute, Department of Endocrinology, Kraepelinstr. 10, D-80804 Munich, Germany

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Rey, Rodolfo. "Endocrine, Paracrine and Cellular Regulation of Postnatal Anti-Müllerian Hormone Secretion by Sertoli Cells." Trends in Endocrinology & Metabolism 9, no. 7 (September 1998): 271–76. http://dx.doi.org/10.1016/s1043-2760(98)00069-1.

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Gromada, Jesper, Isobel Franklin, and Claes B. Wollheim. "α-Cells of the Endocrine Pancreas: 35 Years of Research but the Enigma Remains." Endocrine Reviews 28, no. 1 (February 1, 2007): 84–116. http://dx.doi.org/10.1210/er.2006-0007.

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Glucagon, a hormone secreted from the α-cells of the endocrine pancreas, is critical for blood glucose homeostasis. It is the major counterpart to insulin and is released during hypoglycemia to induce hepatic glucose output. The control of glucagon secretion is multifactorial and involves direct effects of nutrients on α-cell stimulus-secretion coupling as well as paracrine regulation by insulin and zinc and other factors secreted from neighboring β- and δ-cells within the islet of Langerhans. Glucagon secretion is also regulated by circulating hormones and the autonomic nervous system. In this review, we describe the components of the α-cell stimulus secretion coupling and how nutrient metabolism in the α-cell leads to changes in glucagon secretion. The islet cell composition and organization are described in different species and serve as a basis for understanding how the numerous paracrine, hormonal, and nervous signals fine-tune glucagon secretion under different physiological conditions. We also highlight the pathophysiology of the α-cell and how hyperglucagonemia represents an important component of the metabolic abnormalities associated with diabetes mellitus. Therapeutic inhibition of glucagon action in patients with type 2 diabetes remains an exciting prospect.

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Rastelli, Marialetizia, Patrice D. Cani, and Claude Knauf. "The Gut Microbiome Influences Host Endocrine Functions." Endocrine Reviews 40, no. 5 (May 13, 2019): 1271–84. http://dx.doi.org/10.1210/er.2018-00280.

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AbstractThe gut microbiome is considered an organ contributing to the regulation of host metabolism. Since the relationship between the gut microbiome and specific diseases was elucidated, numerous studies have deciphered molecular mechanisms explaining how gut bacteria interact with host cells and eventually shape metabolism. Both metagenomic and metabolomic analyses have contributed to the discovery of bacterial-derived metabolites acting on host cells. In this review, we examine the molecular mechanisms by which bacterial metabolites act as paracrine or endocrine factors, thereby regulating host metabolism. We highlight the impact of specific short-chain fatty acids on the secretion of gut peptides (i.e., glucagon-like peptide-1, peptide YY) and other metabolites produced from different amino acids and regulating inflammation, glucose metabolism, or energy homeostasis. We also discuss the role of gut microbes on the regulation of bioactive lipids that belong to the endocannabinoid system and specific neurotransmitters (e.g., γ-aminobutyric acid, serotonin, nitric oxide). Finally, we review the role of specific bacterial components (i.e., ClpB, Amuc_1100) also acting as endocrine factors and eventually controlling host metabolism. In conclusion, this review summarizes the recent state of the art, aiming at providing evidence that the gut microbiome influences host endocrine functions via several bacteria-derived metabolites.

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SWANSON, L. W., P. E. SAWCHENKO, R. W. LIND, and J. H. RHO. "The CRH Motoneuron: Differential Peptide Regulation in Neurons with Possible Synaptic, Paracrine, and Endocrine Outputs." Annals of the New York Academy of Sciences 512, no. 1 The Hypothala (December 1987): 12–23. http://dx.doi.org/10.1111/j.1749-6632.1987.tb24948.x.

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Whitelaw, P. F., C. D. Smyth, C. M. Howles, and S. G. Hillier. "Cell-specific expression of aromatase and LH receptor mRNAs in rat ovary." Journal of Molecular Endocrinology 9, no. 3 (December 1992): 309–12. http://dx.doi.org/10.1677/jme.0.0090309.

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ABSTRACT Current understanding of the endocrine and paracrine regulation of follicular oestrogen synthesis predicts that aromatase cytochrome P450 (P450arom) mRNA is inducible by FSH in granulosa cells. LH receptor mRNA is constitutively expressed in thecal/interstital cells, and is also thought to be induced in granulosa cells in response to joint stimulation by FSH and oestrogen. This study provides direct evidence that FSH induces the ovarian P450arom gene selectively, perhaps exclusively, in the granulosa cells of Graafian follicles. FSH-induction of LH receptor mRNA occurs simultaneously but is independent of oestrogen synthesis per se.

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Aguilar, Martin, Robert A. Rose, Abhijit Takawale, Stanley Nattel, and Svetlana Reilly. "New aspects of endocrine control of atrial fibrillation and possibilities for clinical translation." Cardiovascular Research 117, no. 7 (March 16, 2021): 1645–61. http://dx.doi.org/10.1093/cvr/cvab080.

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Abstract Hormones are potent endo-, para-, and autocrine endogenous regulators of the function of multiple organs, including the heart. Endocrine dysfunction promotes a number of cardiovascular diseases, including atrial fibrillation (AF). While the heart is a target for endocrine regulation, it is also an active endocrine organ itself, secreting a number of important bioactive hormones that convey significant endocrine effects, but also through para-/autocrine actions, actively participate in cardiac self-regulation. The hormones regulating heart-function work in concert to support myocardial performance. AF is a serious clinical problem associated with increased morbidity and mortality, mainly due to stroke and heart failure. Current therapies for AF remain inadequate. AF is characterized by altered atrial function and structure, including electrical and profibrotic remodelling in the atria and ventricles, which facilitates AF progression and hampers its treatment. Although features of this remodelling are well-established and its mechanisms are partly understood, important pathways pertinent to AF arrhythmogenesis are still unidentified. The discovery of these missing pathways has the potential to lead to therapeutic breakthroughs. Endocrine dysfunction is well-recognized to lead to AF. In this review, we discuss endocrine and cardiocrine signalling systems that directly, or as a consequence of an underlying cardiac pathology, contribute to AF pathogenesis. More specifically, we consider the roles of products from the hypothalamic-pituitary axis, the adrenal glands, adipose tissue, the renin–angiotensin system, atrial cardiomyocytes, and the thyroid gland in controlling atrial electrical and structural properties. The influence of endocrine/paracrine dysfunction on AF risk and mechanisms is evaluated and discussed. We focus on the most recent findings and reflect on the potential of translating them into clinical application.

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Lui, Julian C. "Home for a rest: stem cell niche of the postnatal growth plate." Journal of Endocrinology 246, no. 1 (July 2020): R1—R11. http://dx.doi.org/10.1530/joe-20-0045.

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The resting zone houses a group of slowly proliferating ‘reserve’ chondrocytes and has long been speculated to serve as the stem cell niche of the postnatal growth plate. But are these resting chondrocytes bona fide stem cells? Recent technological advances in lineage tracing and next-generation sequencing have finally allowed researchers to answer this question. Several recent studies have also shed light into the signaling pathways and molecular mechanisms involved in the maintenance of resting chondrocytes, thus providing us with important new insights into the role of the resting zone in the paracrine and endocrine regulation of childhood bone growth.

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Kwaśniewski, Wojciech, Józef Kotarski, Grzegorz Polak, Anna Goździcka-Józefiak, and Jan Kotarski. "The Role of Human Insulin Growth Factor (Igf) – Axis in Carcinogenesis." Advances in Cell Biology 4, no. 1 (March 1, 2014): 25–42. http://dx.doi.org/10.2478/acb-2014-0002.

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Summary The human insulin-like growth factor (IGF) system has attracted significant researcher interest due to its endocrine and autocrine / paracrine activities, mitogenic effects and the involvement in the regulation of proliferation, differentiation and apoptosis. The signaling pathways used by the IGF system impact cellular metabolism in a complex manner complex and many details are still unclear. Understanding the molecular mechanism of action of IGF’s and their effects on cellular activity may provide a basis to develop new anticancer drugs. This review focuses on recent studies that expand our knowledge of the signaling pathways of IGF system

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Roser, Janet F. "Regulation of testicular function in the stallion: An intricate network of endocrine, paracrine and autocrine systems." Animal Reproduction Science 107, no. 3-4 (September 2008): 179–96. http://dx.doi.org/10.1016/j.anireprosci.2008.05.004.

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Thomas, John A. "Drugs and Chemicals that Affect the Endocrine System." International Journal of Toxicology 17, no. 2 (February 1998): 129–38. http://dx.doi.org/10.1080/109158198226666.

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The mammalian endocrine system is very dynamic, and undergoes frequent physiological fluctions due to diurnal variations and cyclical hormonal feedback systems. Both hormonal modulations and chemicall drug perturbations can affect the reproductive systems in males and females. An endocrine disrup-tor, a contemporary term that has been used to define an agent that disrupts the endocrine system, is a hormone or antihormone mimic that can modulate endocrine signaling pathways. Unfortunately, this terminology is confusing and ambiguous and fails to account for the ever-changing endogenous hormonal milieu. The endocrine system can be disrupted or modulated by many physiologic events (e.g., exercise, menstruation, pregnancy), by pharm acologic intervention (e.g., oral contraceptives, antithyroidal medication), and by nutritional states (e.g., iodine deficiencies, vitamin deficiencies and malnutrition). Seasonal changes (e.g., light and temperature) can also modulate endocrine events. Phytoestrogens and xenoestrogens (e.g., chlorinated pesticides) can also affect the dynamics of the endocrine system. Heavy metals and certain anti-cancer agents can interfere with testicular and ovarian function and may cause sterility. Several sites of action can be involved between a drug/chemical and the endocrine system, including the central nervous system, specific target organs or subpopulation of cells, hormone-transporting proteins, and xenobi-otic-m etabolizing enzymes in the liver. At the endocrine target organ level, mechanism(s) of action may involve competition for a cell receptor or affect non-receptor-mediated actions. Some drug!chemicals may act as hormone agonists (i.e., mimic) or conversely act as hormone antagonists (i.e., an antihormone); other agents may act as partial agonists or partial antagonists. Clearly, there are many internal and external factors that can modulate the endocrine system, yet the paracrine and autocrine regulation of specific target organs is finely regulated, and, importantly, is very resilient to drugl chemical perturbation.

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Huhtaniemi, I. "Molecular aspects of the ontogeny of the pituitary-gonadal axis." Reproduction, Fertility and Development 7, no. 5 (1995): 1025. http://dx.doi.org/10.1071/rd9951025.

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The endocrine function of the mammalian pituitary-gonadal axis begins in utero. This is important particularly for the ontogeny and function of the male reproductive organs, the induction of which is critically dependent on the two fetal testicular hormones, testosterone and anti-mullerian hormone. In contrast, ovarian endocrine activity begins only after birth. The earliest phases of testicular hormone production are probably under autocrine or paracrine regulation, but the dependence on gonadotrophins starts in fetal life. During maturation of the hypothalamic-pituitary-testicular axis, the target organs acquire their responsiveness (viz receptors) before the onset of secretion of the tropic hormonal stimulus. The last link to develop is the feedback regulation, and the whole axis is functional in the developing male rat during the last days of gestation. Although gonadotrophin secretion starts in both sexes simultaneously, the fetal ovary is endocrinologically quiescent--its gonadotrophin responsiveness and endocrine activity begin only after birth. The fetal and postnatal periods of testicular activity have crucial effects on male sexual differentiation, whereas in the female, early sexual development occurs autonomously without influence of ovarian function. The purpose of this review is to elucidate some of the recent findings on the molecular mechanisms involved in the perinatal maturation of the rat hypothalamic-pituitary-gonadal axis.

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Hansen, Lene, Bolette Hartmann, Thue Bisgaard, Hitoshi Mineo, Peer N. Jørgensen, and Jens J. Holst. "Somatostatin restrains the secretion of glucagon-like peptide-1 and -2 from isolated perfused porcine ileum." American Journal of Physiology-Endocrinology and Metabolism 278, no. 6 (June 1, 2000): E1010—E1018. http://dx.doi.org/10.1152/ajpendo.2000.278.6.e1010.

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Suspecting that paracrine inhibition might influence neuronal regulation of the endocrine L cells, we studied the role of somatostatin (SS) in the regulation of the secretion of the proglucagon-derived hormones glucagon-like peptide-1 and -2 (GLP-1 and GLP-2). This was examined using the isolated perfused porcine ileum stimulated with acetylcholine (ACh, 10− 6M), neuromedin C (NC, 10− 8 M), and electrical nerve stimulation (NS) with or without α-adrenergic blockade (phentolamine 10− 5 M), and perfusion with a high-affinity monoclonal antibody against SS. ACh and NC significantly increased GLP secretion, whereas NS had little effect. SS immunoneutralization increased GLP secretion eight- to ninefold but had little influence on the GLP responses to ACh, NC, and NS. Basal SS secretion (mainly SS28) was unaffected by NS alone. Phentolamine + NS and NC abstract strongly stimulated release mainly of SS14, whereas ACh had little effect. Infused intravascularly, SS14 weakly and SS28 strongly inhibited GLP secretion. We conclude that GLP secretion is tonically inhibited by a local release of SS28 from epithelial paracrine cells, whereas SS14, supposedly derived from enteric neurons, only weakly influences GLP secretion.

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Moor, Matthias B., and Olivier Bonny. "Ways of calcium reabsorption in the kidney." American Journal of Physiology-Renal Physiology 310, no. 11 (June 1, 2016): F1337—F1350. http://dx.doi.org/10.1152/ajprenal.00273.2015.

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The role of the kidney in calcium homeostasis has been reshaped from a classic view in which the kidney was regulated by systemic calcitropic hormones such as vitamin D3 or parathyroid hormone to an organ actively taking part in the regulation of calcium handling. With the identification of the intrinsic renal calcium-sensing receptor feedback system, the regulation of paracellular calcium transport involving claudins, and new paracrine regulators such as klotho, the kidney has emerged as a crucial modulator not only of calciuria but also of calcium homeostasis. This review summarizes recent molecular and endocrine contributors to renal calcium handling and highlights the tight link between calcium and sodium reabsorption in the kidney.

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Kahn, Darcy E., and Bryan C. Bergman. "Keeping It Local in Metabolic Disease: Adipose Tissue Paracrine Signaling and Insulin Resistance." Diabetes 71, no. 4 (March 22, 2022): 599–609. http://dx.doi.org/10.2337/dbi21-0020.

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Alterations in adipose tissue composition and function are associated with obesity and contribute to the development of type 2 diabetes. While the significance of this relationship has been cemented, our understanding of the multifaceted role of adipose tissue in metabolic heath and disease continues to evolve and expand. Heterogenous populations of cells that make up adipose tissue throughout the body generate diverse secretomes containing a mosaic of bioactive compounds with vast structural and signaling capabilities. While there are many reports highlighting the important role of adipose tissue endocrine signaling in insulin resistance and type 2 diabetes, the direct, local, paracrine effect of adipose tissue has received less attention. Recent studies have begun to underscore the importance of considering anatomically discrete adipose depots for their specific impact on local microenvironments and metabolic function in neighboring tissues as well as regulation of whole-body physiology. This article highlights the important role of adipose tissue paracrine signaling on metabolic function and insulin sensitivity in nearby tissues and organs, specifically focusing on visceral, pancreatic, subcutaneous, intermuscular, and perivascular adipose tissue depots.

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Parrettini, Sara, Massimiliano Cavallo, Francesco Gaggia, Riccardo Calafiore, and Giovanni Luca. "Adipokines: A Rainbow of Proteins with Metabolic and Endocrine Functions." Protein & Peptide Letters 27, no. 12 (December 2, 2020): 1204–30. http://dx.doi.org/10.2174/0929866527666200505214555.

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Obesity represents one of the most important health problems worldwide with increasing morbidity and mortality. Widespread prevalence of this disease justifies its actual definition of a “global epidemic”. Adipose tissue is nowadays considered a complex organ with lots of endocrine and metabolic functions. In addition to fulfilling its task for energy storage and thermal regulation, by virtue of its constituent white and brown cells, adipose tissue represents, considering its size, the biggest endocrine gland in the body. Both adipocytes and surrounding resident cells (macrophages, endothelial cells and others) produce a huge number of molecules, or adipokines, with endocrine or paracrine functions, that regulate various aspects of metabolism whose clinical relevance is emerging. By balancing pro-inflammatory and anti-inflammatory effects, the adipokines control insulin sensitivity and related glucose metabolism changes, lipid accumulation in the liver and other organs, and finally gonadal function. Collectively, literature data remains cloudy because of still conflicting results of pre-clinical and clinical studies. The aim of this review was to summarize scientific evidence about adipokines’ effects on human metabolism, by focusing on their role on either Metabolic Syndrome and NAFLD, or insulin-resistance in pregnancy, or finally, reproductive function disorders.

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Cici, Daniela, Addolorata Corrado, Cinzia Rotondo, Ripalta Colia, and Francesco Paolo Cantatore. "Adipokines and Chronic Rheumatic Diseases: from Inflammation to Bone Involvement." Clinical Reviews in Bone and Mineral Metabolism 18, no. 4 (December 2020): 58–71. http://dx.doi.org/10.1007/s12018-021-09275-w.

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AbstractBesides its well-known role as energy storage tissue, adipose tissue is a biologically active tissue that can also be considered as an endocrine organ, as it is able to secrete adipokines. These bioactive factors, similar in structure to cytokines, are involved in several physiological and pathological conditions, such as glucose homeostasis, angiogenesis, blood pressure regulation, control of food intake, and also inflammation and bone homeostasis via endocrine, paracrine, and autocrine mechanisms. Given their pleiotropic functions, the role of adipokines has been evaluated in chronic rheumatic osteoarticular inflammatory diseases, particularly focusing on their effects on inflammatory and immune response and on bone alterations. Indeed, these diseases are characterized by different bone complications, such as local and systemic bone loss and new bone formation. The aim of this review is to summarize the role of adipokines in rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis, osteoarthritis, and osteoporosis, especially considering their role in the pathogenesis of bone complications typical of these conditions.

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García, María C., Miguel López, Clara V. Alvarez, Felipe Casanueva, Manuel Tena-Sempere, and Carlos Diéguez. "Role of ghrelin in reproduction." Reproduction 133, no. 3 (March 2007): 531–40. http://dx.doi.org/10.1530/rep-06-0249.

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Ghrelin, the endogenous ligand of GH secretagogue receptor type 1a, has emerged as a pleiotropic modulator of diverse biological functions, including energy homeostasis and, lately reproduction. Here, we review recent reports evaluating the reproductive effects and sites of action of ghrelin, with particular emphasis regarding its role as a molecule integrating reproductive function and energy status. Data gleaned from rodent studies clearly show that besides having direct gonadal effects, ghrelin may participate in the regulation of gonadotropin secretion and it may influence the timing of puberty. In addition, experimental data showing that ghrelin and/or its receptor are expressed in normal human ovary and testis as well as in human ovarian and testicular tumors raise the possibility that the ghrelin system may be involved in the control of cell proliferation in these tumors. We propose that ghrelin either acting as an endocrine and/or paracrine signal may play a major role in the endocrine network that integrates energy balance and reproduction.

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Smolinska, N., T. Kaminski, G. Siawrys, and J. Przala. "Ontogeny of the long form of leptin receptor gene expression in the porcine ovarian follicles." Polish Journal of Veterinary Sciences 16, no. 1 (March 1, 2013): 101–5. http://dx.doi.org/10.2478/pjvs-2013-0014.

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Abstract Leptin is a polypeptide hormone produced predominantly in adipocytes. It has been found to be implicated in the regulation of satiety and energy homeostasis. A role for leptin in reproduction was later suggested by findings that this hormone may be involved in the regulation of the hypothalamic- pituitary-gonadal axis via endocrine, paracrine and/or autocrine pathways. The objective of the study was to investigate the ontogeny of the long isoform of leptin receptor (OB-Rb) gene in porcine ovarian follicles. The expression of OB-Rb gene was detected in porcine primordial, primary, secondary and antral follicles by in situ hybridization. In summary, our data suggest that leptin might have a direct effect on porcine follicles and plays an important role in the follicular development.

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Journal articles on the topic 'Endocrine and paracrine regulations'

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