Готові списки джерел за темами / Insulin metabolism

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Добірка наукової літератури з теми "Insulin metabolism"

Автор: Grafiati
Опубліковано: 4 червня 2021
Оновлено: 20 лютого 2023

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Статті в журналах з теми "Insulin metabolism"

1

Ukkola, O. "Ghrelin and insulin metabolism." European Journal of Clinical Investigation 33, no. 3 (March 2003): 183–85. http://dx.doi.org/10.1046/j.1365-2362.2003.01112.x.

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2

Duckworth, William C., Frederick G. Hamel, and Daniel E. Peavy. "Hepatic metabolism of insulin." American Journal of Medicine 85, no. 5 (November 1988): 71–76. http://dx.doi.org/10.1016/0002-9343(88)90399-3.

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3

Heesom, K. J., M. Harbeck, C. R. Kahn, and R. M. Denton. "Insulin action on metabolism." Diabetologia 40 (September 19, 1997): S3—S9. http://dx.doi.org/10.1007/s001250051388.

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4

Beardsall, Kathryn, Barbro M. S. Diderholm, and David B. Dunger. "Insulin and carbohydrate metabolism." Best Practice & Research Clinical Endocrinology & Metabolism 22, no. 1 (February 2008): 41–55. http://dx.doi.org/10.1016/j.beem.2007.10.001.

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5

Heesom, K. J., M. Harbeck, C. R. Kahn, and R. M. Denton. "Insulin action on metabolism." Diabetologia 40, S3 (March 1997): B3—B9. http://dx.doi.org/10.1007/bf03168179.

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6

Harned, Leighton Kahle, and Edward Chin. "PSUN278 Factitious hypoglycemia, diagnostic delay due to insulin assay failure to detect insulin analogues." Journal of the Endocrine Society 6, Supplement_1 (November 1, 2022): A403. http://dx.doi.org/10.1210/jendso/bvac150.838.

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Abstract Factitious hypoglycemia may be difficult to diagnose clinically. Hypoglycemia due to insulin self-administration is established by the presence of a low c-peptide and elevated plasma insulin levels. Commercial insulin assays often fail to detect insulin analogs and can create confusion among providers investigating causes of hypoglycemia. A 20 year old female with no significant past medical history presented to an Emergency Room (ER) with hypoglycemia. She was treated with a single dose of octreotide 150 mcg, dexamethasone 10 mg PO and started on a D10W drip at 100ml/hr prior to transfer. Laboratory studies on transfer reported plasma glucose 52ng/dL (RR: 70-100), low C-peptide 0.02 (RR: 0.78-5.19), low insulin level <0.087 uIU/mL, normal IGF-I level 122 ng/mL (RR: 85-370). Normal IGF-II level 401 ng/mL (RR: 333-967), and low Pro-insulin level 1.8 pmol/L (RR: 3.6-22 pmol/L). Sulfonylurea Screen was negative. The patient and her mother both denied exogenous insulin use. The patient and her mother both work in healthcare. The patient's boyfriend has type 1 diabetes mellitus and the patient stated she keeps insulin in her purse for him. The patient was admitted for a 72 hour fast and remained normoglycemic. An aliquot of the admission ER insulin blood sample was sent to second laboratory utilizing an assay able to detect analog insulins. The patient's sample previously reporting an undetectable insulin level (<0.087 uIU/mL) now reported an insulin level 8 uIU/mL. Factitious hypoglycemia is a challenging clinical diagnosis. The term factitious implies an attempt to deceive and creates mistrust between the physician and patient. However, hypoglycemia may be the result of medication errors or administered by a second party with the intent to harm. Analog insulins (glargine, aspart, lispro, glulisine, etc) are genetically modified insulins developed to mimic the physiologic pattern of pancreatic beta cell insulin secretion. The amino acid modifications in analog insulins result in structural variations which alters the ability of highly specific commercial automated immunoassays to accurately quantitate these analog insulins. The variation in lab assay detection may cause confusion when interpreting the results. The DiaSorin Liaison XL platform in our hospital utilizes a chemiluminescence immunoassay which does not detect insulin analogs, but detects regular and NPH insulin as they are structurally identical to endogenous human insulin. The second laboratory uses the Siemens Advia Centaur platform, an immunoassay which reacts with insulin analogs "on a nearly equimolar basis with the analogs insulin aspart, insulin glargine, and insulin lispro. Insulin detemir exhibits approximately 50 percent cross-reactivity. Test reactivity with insulin glulisine is negligible (< 3 percent)". Many commercial insulin assays do not detect analog insulins and none qualitatively distinguish between different insulins. Failure to recognize this detection flaw may result in misdiagnosis, patient safety issues and costly unneeded additional studies Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.
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7

Kagotho, Elizabeth. "Insulin-Mediated Glucose Metabolism: An Atherogenic Lipid Profile of Fructose Consumption." Endocrinology and Disorders 2, no. 2 (February 27, 2018): 01–02. http://dx.doi.org/10.31579/2640-1045/096.

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Our laboratory has investigated two hypotheses regarding the effects of fructose consumption: 1) The endocrine effects of fructose consumption favor a positive energy balance, and 2) Fructose consumption promotes the development of an atherogenic lipid profile. In previous short- and long-term studies, we demonstrated that consumption of fructose-sweetened beverages with 3 meals results in lower 24-hour plasma concentrations of glucose, insulin, and leptin in humans compared with consumption of glucose-sweetened beverages. We have also tested whether prolonged consumption of high-fructose diets could lead to increased caloric intake or decreased energy expenditure, thereby contributing to weight gain and obesity. Results from a study conducted in rhesus monkeys produced equivocal results. Carefully controlled and adequately powered long-term studies are needed to address these hypotheses. In both short- and long-term studies we demonstrated that consumption of fructose-sweetened beverages substantially increases postprandial triacylglycerol concentrations compared with glucose-sweetened beverages. In the long-term studies, apolipoproteinB concentrations were also increased in subjects consuming fructose, but not those consuming glucose. Data from a short-term study comparing consumption of beverages sweetened with fructose, glucose, high fructose corn syrup (HFCS) and sucrose, suggest that HFCS and sucrose increase postprandial triacylglycerol to an extent comparable to that induced by 100% fructose alone. Increased consumption of fructose-sweetened beverages along with increased prevalence of obesity, metabolic syndrome, and type 2 diabetes underscore the importance of investigating the metabolic consequences fructose consumption in carefully controlled experiments.
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8

Kagotho, Elizabeth. "Insulin-Mediated Glucose Metabolism: An Atherogenic Lipid Profile of Fructose Consumption." Endocrinology and Disorders 2, no. 2 (February 15, 2018): 01–02. http://dx.doi.org/10.31579/2640-1045/021.

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9

Kusters, Yvo H. A. M., and Eugene J. Barrett. "Muscle microvasculature's structural and functional specializations facilitate muscle metabolism." American Journal of Physiology-Endocrinology and Metabolism 310, no. 6 (March 15, 2016): E379—E387. http://dx.doi.org/10.1152/ajpendo.00443.2015.

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We review the evolving findings from studies that examine the relationship between the structural and functional properties of skeletal muscle's vasculature and muscle metabolism. Unique aspects of the organization of the muscle microvasculature are highlighted. We discuss the role of vasomotion at the microscopic level and of flowmotion at the tissue level as modulators of perfusion distribution in muscle. We then consider in some detail how insulin and exercise each modulate muscle perfusion at both the microvascular and whole tissue level. The central role of the vascular endothelial cell in modulating both perfusion and transendothelial insulin and nutrient transport is also reviewed. The relationship between muscle metabolic insulin resistance and the vascular action of insulin in muscle continues to indicate an important role for the microvasculature as a target for insulin action and that impairing insulin's microvascular action significantly affects body glucose metabolism.
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10

Piloquet, H., V. Ferchaud-Roucher, F. Duengler, Y. Zair, P. Maugere, and M. Krempf. "Insulin effects on acetate metabolism." American Journal of Physiology-Endocrinology and Metabolism 285, no. 3 (September 2003): E561—E565. http://dx.doi.org/10.1152/ajpendo.00042.2003.

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Acetate metabolism was studied in patients with insulin resistance. To evaluate the interaction between glucose and acetate metabolism, we measured acetate and glucose turnover with a hyperinsulinemic euglycemic clamp (hot clamp) in obese and diabetic patients with insulin resistance ( n = 8) and in a control group with normal insulin sensitivity ( n = 6). At baseline, acetate turnover and plasma concentrations were similar between the two groups (group means: 4.3 ± 0.4 μmol · kg-1 · min-1 and 128.2 ± 11.1 μmol/l). Acetate concentrations decreased in both groups with hyperinsulinemia but were significantly lower in the insulin-resistant group (20% vs. 12%, P < 0.05). After the hot clamp treatment, acetate turnover increased for the two groups and was higher in the group with normal insulin sensitivity: 8.1 ± 0.7 vs. 5.5 ± 0.5 μmol · kg-1 · min-1 ( P < 0.001). No change related to insulin action was observed in either group in the percentage of acetate oxidation. This was ≈70% of overall utilization at baseline and during the clamp. No correlation between glucose and acetate utilization was observed. Our results support the hypothesis that, like glucose metabolism, acetate metabolism is sensitive to insulin.
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Дисертації з теми "Insulin metabolism"

1

Vidal, Alabró Anna. "Estudi de l’activació de la glucocinasa (GKA456V) en fetge perivenós." Doctoral thesis, Universitat de Barcelona, 2011. http://hdl.handle.net/10803/32022.

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La GK és clau en la regulació del metabolisme glucídic tant per la seva funció al pàncrees en què determina la secreció d’insulina, com per la seva funció al fetge on controla les vies d’utilització i d’emmagatzematge de glucosa. Per aquest motiu és una bona diana per a la teràpia de la diabetis, i diverses companyies farmacèutiques estan desenvolupant activadors sintètics de la GK (GKA) pel tractament de la diabetis de tipus 2. Els estudis de GKAs existents avaluen l’activació de la GK a nivell sistèmic i no es coneixen els seus efectes específis sobre la GK al fetge. Per indagar-los, com que no disposàvem d’un GKA específic per a la GK del fetge, ens vam proposar la sobrexpressió d’una forma de GK amb una mutació activadora (GK-A456V) que confereix característiques cinètiques a l’enzim idèntiques a les obtingudes amb els GKAs. L’introduírem al fetge perivenós mitjançant transfecció gènica hidrodinàmica (perquè és la zona on s’expressa majoritàriament l’enzim salvatge en condicions fisiològiques). Un dels controls emprats en l’estudi fou la sobrexpressió de la GK salvatge també a la zona perivenosa, que ens permetria comparar els resultats d’aquesta sobrexpressió local de la GK amb la sobrexpressió no zonal descrita a la bibliografia. Per una banda, avaluàrem els efectes de la sobrexpressió i de l’activació de la GK hepàtica en el context d’un animal sa a llarg termini, per determinar si hi havia risc de resistència a insulina (com s’esdevé en alguns models de sobrexpressió no zonal de GK al fetge). Tant l’activació com la sobrexpressió de GK al fetge perivenós a curt termini comportaren una disminució de la glicèmia i de la insulinèmia. No obstant, en avaluar-ho a llarg termini, la sobrexpressió de GK generà un fenotip de resistència a insulina exclusivament al fetge. En canvi, la GK-A456V comportà un fenotip amb un perfil metabòlic similar als animals controls, sense alteracions dels nivells de glúcids i lípids (sèrics i hepàtics). Al fetge, malgrat que no provocava canvis en el metabolisme glucídic i lipídic, l’activació de la GK va promoure la desregulació per GKRP i la inducció de la glucosa-6-fosfatasa. Per altra banda, la presència de la GK activada al fetge resultà en una activació del catabolisme al teixit adipós. Per altra banda, vam emprar un model de diabetis de tipus 1 per determinar els efectes de la GK-A456V sobre el fenotip diabètic independentment de la insulina, amb la finalitat de valorar l’activació de la GK hepàtica com a tractament alternatiu als GKAs sistèmics. La sobrexpressió perivenosa de GK, tot i que comportà un increment del metabolisme de glucosa al fetge (increment del glicogen hepàtic, de ub-PFK-2, de L-PK, c-myc) i una disminució de la gluconeogènesi (reducció dels nivells de PEPCK), va provocar dislipidèmia com a resultat de la disminució de la β-oxidació d’àcids grassos (reducció dels nivells de Cpt-1) i una inducció de la lipogènesi hepàtica (augment de FAS, ACC, ChREBP). Altres models de sobrexpressió de GK, descrits a la literatura, que no tenien en compte el concepte de zonació hepàtica, també presentaven alteracions en el metabolisme lipídic. En canvi, l’activació de la GK comportà una rellevant disminució de la hiperglicèmia diabètica tot i tenir un lleu efecte sobre l’activació del metabolisme de glucosa i sobre la inhibició de la gluconeogènesi. Sobretot és interessant que la millora de la hiperglicèmia diabètica no va acompanyada d’alteracions del metabolisme lipídic. En conjunt, aquest treball suggereix que l’activació de la GK exclusivament al fetge és una estratègia terapèutica millor per a la diabetis que la sobrexpressió de la GK.
Synthetic glucokinase activators have been used in the context of type 2 diabetes therapy, mainly for their insulin secretagogue activity. However, the impact of these drugs on liver GK has not been studied in vivo. Since GK activators and activating GK mutations confer identical kinetic properties to GK, we hypothesize that hepatic overexpression of a mutated form of GK, GKA456V, described in a patient with Persistent Hyperinsulinemic Hypoglycemia of Infancy (PHHI), shall mimic the liver-specific effects of GK-activating drugs. GKA456V was overexpressed in the liver of streptozotocin diabetic mice and also in healthy mice. Metabolite profiling in serum and liver extracts, together with key components of glucose and lipid homeostasis, were analyzed and compared to GK wild-type transfected animals. Cell compartmentalization of mutant and wild-type GK was also examined in vivo. In the type 1 diabetic mice, GKA456V overexpression markedly reduced blood glucose in the absence of dislipidemia, in contrast to wild-type GK-overexpressing mice. Enhanced glucose utilization did not correlate with glycogen synthesis or lactate production. PEPCK mRNA was not affected, whereas the mRNA for the catalytic subunit of glucose-6-phosphatase was upregulated ~4-fold in the liver of GKA456V treated animals. Moreover, GKA456V was not translocated to the nucleus after a short fast, confirming that this activating mutation disrupted GKRP regulation. In healthy mice, the overexpression of hepatic GK resulted in insulin resistance. Otherwise, GKA456V overepxressing animals were not insulin resistant. They showed increased mRNA and protein content of the catalytic subunit of glucose-6-phosphatase in the liver, and an idnuction of catabolism in their adipose tissue. Our results validate liver specific GK activation as a strategy for diabetes therapy and provide new insights into the complex GK regulatory network.
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2

Collison, Mary Williamson. "Insulin signalling in insulin resistance and cardiovascular disease syndromes." Thesis, University of Glasgow, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.366184.

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3

Kershner, David. "Oral Glucose Insulin Secretion Test for Identifying Patients with Insulin Resistance." ScholarWorks, 2018. https://scholarworks.waldenu.edu/dissertations/5634.

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Insulin resistance is an increasing public health issue with the current literature, suggesting reduced sensitivity of insulin leads to adult onset diabetes and associated downstream pathologies that reduce life expectancy. The main objectives of this study were to evaluate the ability of the Oral Glucose Insulin Secretion Test (OGIST) to identify insulin resistance and examine differences in the insulin sensitivity based on gender, age, and ethnicity. This study was supported by the insulin resistance theory which focuses on the reduced ability of insulin to bind to the cellular insulin receptor, reducing the sensitivity of insulin. The OGIST lab results of a total of 250 patients, aged 18-65, were included in this study from a major city in the midwestern United States. Binomial logistic regression was used to evaluate the relationship between the dependent variables and the validation independent variables and analyze the possible differences seen in insulin, proinsulin, C-peptide, and HbA1c with age. The OGIST demonstrated the ability to identify elevated levels of insulin, proinsulin, and C-peptide at the end of the first phase insulin secretion to glucose. The results of this study demonstrated patients with insulin resistance exhibited a greater reduction in insulin production with age compared to those without insulin resistance. There were no changes observed between gender or ethnicity. The OGIST was the only test that demonstrated the ability to identify the individual's insulin sensitivity, β-cell function, and progression to diabetes. The ability of the OGIST to identify both insulin resistance and β-cell function can contribute to positive social change by encouraging further research for the early diagnosis and treatment of insulin resistance and the reduction in adult onset diabetes.
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4

Mashhedi, Haider. "Implicating insulin in neoplastic growth and metabolism." Thesis, McGill University, 2011. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=104681.

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In view of accumulating evidence that links obesity to increased cancer burden, there is interest in delineating the mechanisms by which obesity influences neoplastic growth. Increased insulin levels are commonly associated with obesity or ‘the metabolic syndrome' and thus the insulin receptor has been viewed as a potentially important molecular target for the treatment of certain cancers. To study the effects of insulin signaling attenuation on the growth of the experimental insulin-responsive mouse 4T1 breast cancer cells in vivo, we compared the effects of alloxan-induced insulin deficiency to that of BMS-536924, an inhibitor of the insulin and IGF-I receptor tyrosine kinases. Both interventions displayed anti-neoplastic activity, while metabolic toxicity resulted only from alloxan. Insulin receptor inhibition did not result in severe hyperglycemia and treatment with BMS-536924 was well tolerated. We attributed this to pharmacokinetic factors by measuring drug tissue accumulation and measuring glucose utilization in muscle to determine if BMS-536924 abolished insulin-dependent glucose uptake. Our data indicate that insulin dependent glucose uptake by muscle remained intact. Thus, tissue-specific distribution of BMS- 536924 may account for anti-neoplastic activity without severe metabolic toxicity, indicating that pharmacologic targeting of the insulin receptor in neoplastic disease may be practical.Population studies have shown that type II diabetic patients on the biguanide drug metformin have a reduced risk of cancer development or mortality from cancer compared to type II diabetic patients on other therapies. We previously showed that metformin acts as a growth inhibitor in tumor cells in vitro by increasing AMPK phosphorylation in a dose-dependent manner. AMPK activation by metformin, which is seen in tumor cells both in vitro and in vivo, also decreases circulating insulin levels as a secondary effect to lowering blood glucose levels in a setting of type II diabetes. Positron-emission tomography (PET) is an imaging technique that measures the glucose utilization rate that takes place in cancer cells by using the radiolabeled glucose analog 18F-2-Fluoro-2-Deoxy-D-Glucose (FDG). We were interested in the effects of metformin on tumor glucose uptake in mice harboring MC38 colon-adenocarcinoma allografts that were fed either a high-energy diet (that induces a type II diabetic phenotype), or a control diet. Our results show that metformin abolished diet-induced increases in serum insulin levels, tumor insulin receptor activation, and tumor FDG uptake associated with mice on the high-energy diet and that metformin had no effect on these measurements in mice on a control diet. This suggests that for a subset of neoplasms, diet and insulin influence tumor glucose uptake, and this may yield clinical relevance in upcoming trials evaluating metformin's anti-neoplastic activity.
Compte tenu de l'accumulation de preuves liant l'obésité à un nombre accru de cancers, il y a un grand intérêt à définir les mécanismes par lesquels l'obésité influe sur la croissance néoplasique. Des niveaux d'insuline élevés sont couramment associés à l'obésité ou au «syndrome métabolique», ce qui fait que le récepteur de l'insuline est considéré comme une cible moléculaire potentiellement importante pour le traitement de certains cancers. Pour étudier les effets de l'atténuation de la signalisation de l'insuline sur la croissance du modèle expérimental du cancer du sein chez la souris, la lignée cellulaire insulino-sensible 4T1 in vivo, nous avons comparé les effets d'une déficience à l'insuline induite par l'alloxan à celle de BMS-536924, un inhibiteur des kinases tyrosine des récepteurs de l'insuline et d'IGF-I. Les deux interventions ont montré une activité anti-néoplasique, mais seulement l'alloxan a présenté une toxicité métabolique. L'inhibition des récepteurs d'insuline n'a occasionné qu'une faible hyperglycémie et le traitement avec BMS-536924 a été bien toléré. Nous avons attribué ce phénomène à des facteurs pharmacocinétiques en mesurant l'accumulation de drogue dans les tissus et pour déterminer si le BMS-536924 abolit l'absorption insulino-dépendante du glucose, nous avons mesuré la quantité de glucose utilisé dans le muscle. Nos données indiquent que la captation insulino-dépendante du glucose par le muscle est restée intacte. Ainsi, la distribution tissu-spécifique du BMS-536924 peut être responsable de l'activité anti-néoplasique sans toxicité métabolique grave, ce qui indique que le ciblage pharmacologique du récepteur de l'insuline dans la maladie néoplasique peut être efficace.Les études épidémiologiques ont montré que les patients diabétiques de type II prenant le médicament metformine (un biguanide) ont un risque réduit de développer un cancer ou d'un taux de mortalité due au cancer plus faible par rapport aux patients diabétiques de type II suivant d'autres thérapies. Nous avons déjà montré que la metformine agit comme un inhibiteur de la croissance des cellules tumorales in vitro en phosphorylant l'AMPK d'une manière dépendante de la dose. Outre l'activation de l'AMPK, qui est observée dans les cellules tumorales in vitro et in vivo, la metformine provoque aussi une diminution des taux d'insuline. Ceci est un effet secondaire de la réduction du taux de glycémie dans un contexte de diabète de type II. La tomographie par émission de positons (TEP ou PET) est une technique d'imagerie qui mesure le taux d'utilisation du glucose par les cellules cancéreuses à l'aide de l'analogue du glucose radiomarqué 18F-2-Fluoro-2-Désoxy-D-Glucose (FDG). Nous étions intéressés par les effets de la metformine sur la captation du glucose par les tumeurs d'adénocarcinome de côlon, MC38, allogreffées chez des souris qui ont été nourris avec une diète à haute teneur énergétique (induisant un phénotype diabétique de type II), ou un régime contrôle. Nos résultats montrent que la metformine abolie l'augmentation des niveaux sériques d'insuline, l'activation du récepteur d'insuline dans les tumeurs ainsi que l'absorption du FDG par les tumeur chez les souris ayant un régime riche en énergie et que la metformine n'a aucun effet sur ces mesures chez les souris ayant une diète contrôle. Ceci suggère que pour un sous-ensemble de néoplasmes, le régime alimentaire et le taux d'insuline influencent l'absorption du glucose par les cellules tumorales ce qui pourrait avoir une pertinence clinique dans les prochaines études clinique visant l'évaluation de l'activité anti-néoplasique de la metformine.
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5

Shmueli, Ehoud. "Glucose metabolism and insulin resistance in cirrhosis." Thesis, University of Newcastle Upon Tyne, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.308777.

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6

Laberge, Marie-Kristine. "Nck1 is required for ER stress-induced insulin resistance and regulation of IRS1-dependent insulin signalling." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111950.

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Activation of the Unfolded Protein Response (UPR) following stress in the Endoplasmic Reticulum (ER) is an important mechanism by which obesity results in insulin resistance and type II diabetes. We uncovered a role for the adaptor protein Nck in modulating the UPR. In this study, we report that obese Nck1-/- mice, which show lower levels of UPR in liver and adipose tissue, present improved insulin signalling in these tissues. We established that the effect of Nck1 is cell autonomous by showing that HepG2 cells treated with Nck1 siRNA have reduced ER stress-induced UPR and Insulin Receptor Substrate-1 (IRS-1) serine phosphorylation. In these cells, we observed that the IRS-1 levels and activation of signalling components downstream of the insulin receptor were increased. This correlates with enhanced cell survival to stress and insulin stimulated glycogen synthesis. Overall, we demonstrated that Nck1 participates in ER-stress-induced insulin resistance and regulation of IRS-1-dependent signalling.
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7

Sanderson, Alison Louise. "Regulation of skeletal muscle metabolism." Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.318615.

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8

Field, Polly Ann. "The effects of insulin resistance on chylomicron metabolism." Thesis, University of Oxford, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.302120.

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9

DeAngelis, Anthony Michael. "CEACAM1 : a link between insulin and lipid metabolism." Connect to full text in OhioLINK ETD Center, 2009. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=mco1243943993.

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Dissertation (Ph.D.)--University of Toledo, 2009.
"In partial fulfillment of the requirements for the degree of Doctor of Philosophy in Biomedical Sciences." Title from title page of PDF document. Bibliography: p. 57-61, p. 20-145.
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10

Nygren, Jonas. "The sites and mechanisms of postoperative insulin resistance /." Stockholm, 1997. http://diss.kib.ki.se/1997/91-628-2695-6.

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Книги з теми "Insulin metabolism"

1

Markussen, Jan. Human insulin by tryptic transpeptidations of porcine insulin and biosynthetic procursors. Lancaster: MTP Press, 1987.

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Human insulin by tryptic transpeptidations of porcine insulin and biosynthetic precursors. Lancaster: MTP Press, 1987.

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3

Joseph, Goren H., Hollenberg Morley D. 1942-, and Roncari Daniel A. K, eds. Insulin action and diabetes. New York: Raven Press, 1988.

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European Symposium on Metabolism (8th 2002 Padua, Italy). The metabolic syndrome: Diabetes, obesity, hyperlipidemia & hypertension : proceedings of the 8th European Symposium on Metabolism, held in Padua, Italy, between 2 and 5 October 2002. Edited by Crepaldi Gaetano, Tiengo Antonio, and Avogaro Angelo. Amsterdam: Elsevier, 2003.

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5

Ṿisut ha-energyah ba-guf: Pereḳ be-endoḳrinologyah. [Tel Aviv]: Maṭkal/Ḳetsin ḥinukh rashi/Gale-Tsahal, Miśrad ha-biṭaḥon, 1985.

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6

Trumbach, Sabine. Glukose-Toleranz und Insulin-Sekretion unter simulierter Schwerelosigkeit. Koln: DFLVR, 1988.

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7

Iwar, Klimes, ed. Dietary lipids and insulin action. New York, N.Y: New York Academy of Sciences, 1993.

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8

Gaetano, Crepaldi, Tiengo Antonio, and Manzato E, eds. Diabetes, obesity, and hyperlipidemias, V: The plurimetabolic syndrome : proceedings of the European Symposium on Metabolism, Padova, 24-26 May 1993. Amsterdam: Excerpta Medica, 1993.

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9

Dorrestijn, Jannette. Signal transduction related to the metabolic action of insulin. [Leiden: University of Leiden, 1998.

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10

1929-, Shigeta Yukio, Kobayashi Masashi Dr, and Olefsky Jerrold M, eds. Recent advances in insulin action and its disorders: Proceedings of the International Symposium on Insulin Action and Its Disorders, Shiga, 16 May 1990. Amsterdam: Excerpta Medica, 1991.

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Частини книг з теми "Insulin metabolism"

1

Larner, J. "Effects of Insulin on Glycogen Metabolism." In Insulin, 367–84. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74098-5_16.

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Bressler, R., and J. J. Bahl. "Insulin Regulation of Metabolism Relevant to Gluconeogenesis." In Insulin, 451–67. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74098-5_20.

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Frayn, Keith N., and Fredrik Karpe. "Insulin Action on Lipid Metabolism." In Insulin Resistance, 87–103. Chichester, UK: John Wiley & Sons, Ltd, 2005. http://dx.doi.org/10.1002/0470011327.ch3.

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Konrad, Daniel, Assaf Rudich, and Amira Klip. "Insulin-Mediated Regulation of Glucose Metabolism." In Insulin Resistance, 63–85. Chichester, UK: John Wiley & Sons, Ltd, 2005. http://dx.doi.org/10.1002/0470011327.ch2.

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Hileman, Stanley M., and Christian Bjørbaek. "Central Regulation of Peripheral Glucose Metabolism." In Insulin Resistance, 179–206. Chichester, UK: John Wiley & Sons, Ltd, 2005. http://dx.doi.org/10.1002/0470011327.ch7.

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Greenlund, Laura J. S., and K. Sreekumaran Nair. "The Effect of Insulin on Protein Metabolism." In Insulin Resistance, 105–32. Chichester, UK: John Wiley & Sons, Ltd, 2005. http://dx.doi.org/10.1002/0470011327.ch4.

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Mathias, Dietger. "Metabolism and Insulin Effect." In Fit and Healthy from 1 to 100 with Nutrition and Exercise, 143. Berlin, Heidelberg: Springer Berlin Heidelberg, 2022. http://dx.doi.org/10.1007/978-3-662-65961-8_67.

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Patnaik, Akash, Jason W. Locasale, and Lewis C. Cantley. "Cancer Cell Metabolism." In Insulin-like Growth Factors and Cancer, 245–61. Boston, MA: Springer US, 2011. http://dx.doi.org/10.1007/978-1-4614-0598-6_13.

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Guest, Paul C. "Insulin Resistance in Schizophrenia." In Reviews on Biomarker Studies of Metabolic and Metabolism-Related Disorders, 1–16. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-12668-1_1.

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Carmena, R., J. F. Ascaso, A. Merchante, and F. J. Ampudia. "Insulin Resistance and Lipid Disorders." In Drugs Affecting Lipid Metabolism, 379–88. Dordrecht: Springer Netherlands, 1996. http://dx.doi.org/10.1007/978-94-009-0311-1_44.

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Тези доповідей конференцій з теми "Insulin metabolism"

1

Senhorinha, Gláucia Maria, Arlys Emanuel Mendes da Silva Santos, and Douglas Daniel Dophine. "The role of metabolic syndrome in Alzheimer’s disease." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.319.

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Background: Metabolic syndrome (MS) leads to the deposits formation of insoluble protein aggregates, neuroinflammation, oxidative stress, neuronal insulin resistance, progressive insulin resistance, desensitization and β-amyloid amyloidosis in the brain, besides direct ischemic effects which are closely associated with Alzheimer’s disease (AD).1 Objectives: The present study seeks to understand the role of the metabolic syndrome in the pathophysiology of Alzheimer’s disease and to describe preventive and therapeutic interventions. Methods: PUBMED and Web of Science were the databases used, the following descriptors were used to search the articles: “Alzheimer Disease” OR “Alzheimer Dementia” AND “Metabolic Syndrome”. Results: The studies in general have shown that MS is related to AD through brain insulin resistance, triggered by oxidative stress and neuroinflammation. It is related to the progressive atrophy of brain regions involved in the progression of AD. Insulin resistance in the brain is related to the progressive atrophy of the brain regions from initial progression of AD. These regions are cingulate cortices, medial temporal lobe, prefrontal gyri and other regions.³ Thus, there is an inhibition of the mechanisms of beta-amyloid removal, leading to its accumulation, which generates neuroinflammation, that in turn potentiates insulin resistance in the central nervous system, contributing to the genesis and progression of cognitive damage.2,3 Conclusions: Insulin resistance plays a major role in the initiation and perpetuation of cognitive impairment in AD. Furthermore, the components of the MS associated with AD, when treated with preventive and therapeutic measures, break this association by promoting rebalancing of the metabolism.
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El-fadl, Rihab, Nasser Rizk, Amena Fadel, and Abdelrahman El Gamal. "The Profile of Hepatic Gene Expression of Glucose Metabolism in Mice on High Fat Diet." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0213.

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Obesity is a growing problem worldwide, and recent data indicated that 20% of the populations would be obese. Obesity arises as a multifactorial disease caused by inherited traits that interact with lifestyle factors such as diet and physical activity. The liver plays an essential role in the gluco-regulation via regulating glucose, lipid and protein metabolism. The process of glucose metabolism is controlled by a range of molecular mechanisms and genes which affect the metabolism of the liver during intake of high fat diet (HFD). The objective of this research is to investigate the profile of hepatic gene expression of glucose metabolism in mice on HFD treated with leptin (5 mg/kg BW Ip injection). Ten wild type CD1 mice fed on HFD is used for this study, where groups are control (vehicle - leptin) and test group (vehicle + leptin). Body weight (BW) was measured, and blood chemistry, insulin and leptin were measured at the end of the experiments. Total RNA was isolated from the liver tissue, and RTPCR profiler array technology was used to evaluate the mRNA expression of 84 essential genes of hepatic glucose metabolism. The data of the BW and blood chemistry are not significantly different between the two groups. Leptin treatment enhanced the metabolic pathways and the candidate genes of the different metabolic pathway; glycogen metabolism such as Gys1, Gys2 and Pygm, pentose phosphate shunt such as Rpia and suppressed the glycolysis such as Aldob, and TCA cycle such as Mdh1b. In conclusion, this study has shown that leptin could affect the profile of the hepatic mouse genes of glucose metabolism in the early stages of HFD to induce obesity
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Rad, Milad Ghiasi, Aditya Immaneni, Megan McCabe, Massimiliano Pierobon, and Juan Cui. "A simulation model of glucose-insulin metabolism and implementation on OSG." In 2017 IEEE International Conference on Bioinformatics and Biomedicine (BIBM). IEEE, 2017. http://dx.doi.org/10.1109/bibm.2017.8217939.

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Staal, Odd Martin, Anders Lyngvi Fougner, Steinar Saelid, and Oyvind Stavdahl. "Glucose-insulin metabolism model reduction and parameter selection using sensitivity analysis." In 2019 American Control Conference (ACC). IEEE, 2019. http://dx.doi.org/10.23919/acc.2019.8814949.

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Wardelmann, K., M. Rath, JP Castro, S. Blümel, M. Schell, R. Hauffe, C. Chudoba, et al. "Central acting Hsp10 regulates mitochondrial function, insulin sensitivity and impacts liver metabolism." In Diabetes Kongress 2021 – 55. Jahrestagung der DDG. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1727356.

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Campos, L. M., A. G. Rius, D. Kirovski, J. A. D. R. N. Appuhamy, T. F. V. Bompadre, and M. D. Hanigan. "Mammary gland amino acid affinity in response to different levels of dietary protein and insulin." In 6th EAAP International Symposium on Energy and Protein Metabolism and Nutrition. The Netherlands: Wageningen Academic Publishers, 2019. http://dx.doi.org/10.3920/978-90-8686-891-9_120.

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Diniz, Clebiana Alves e. silva, Poliana Silva de Brito, Tainan de Andrade Rocha, Suzana Maria de Oliveira Costa Meneses, and Julia Maria Pacheco Lins Magalhães. "Elderly people with diabetes: an analysis of the factors that are associated with lower limb amputation." In II INTERNATIONAL SEVEN MULTIDISCIPLINARY CONGRESS. Seven Congress, 2023. http://dx.doi.org/10.56238/homeinternationalanais-028.

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Abstract Population aging has been occurring extremely rapidlyin developing countries, implying a higher prevalence of chronic-degenerative diseases (NCDs,s). Among these, diabetes mellitus stands out, a syndrome characterized by a chronic state of hyperglycemia and disorders in the metabolism of carbohydrates, lipids and proteins, associated with absolute or relative insulin deficiency and/or its action in the body.
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Mougiakakou, Stavroula G., Aikaterini Prountzou, Dimitra Iliopoulou, Konstantina S. Nikita, Andriani Vazeou, and Christos S. Bartsocas. "Neural Network based Glucose - Insulin Metabolism Models for Children with Type 1 Diabetes." In Conference Proceedings. Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2006. http://dx.doi.org/10.1109/iembs.2006.260640.

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Mougiakakou, Stavroula G., Aikaterini Prountzou, Dimitra Iliopoulou, Konstantina S. Nikita, Andriani Vazeou, and Christos S. Bartsocas. "Neural Network based Glucose - Insulin Metabolism Models for Children with Type 1 Diabetes." In Conference Proceedings. Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2006. http://dx.doi.org/10.1109/iembs.2006.4398212.

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Đokovic, Radojica, Marko Cincovic, Vladimir Kurćubic, Milun D. Petrovic, Miloš Ži Petrovic, Ljiljana Anđušic, and Biljana Anđelic. "HOMEORETSKA REGULACUJA METABOLIČKIH FUNKCIJA KOD KRAVA U PERIPARTALNOM PERIODU." In SAVETOVANJE o biotehnologiji sa međunarodnim učešćem. University of Kragujevac, Faculty of Agronomy, 2021. http://dx.doi.org/10.46793/sbt26.235dj.

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The aim of this paper is to describe complex homeoretic and homeostatic mechanisms in dairy cows during the peripartum period. The endocrine system has a key function in regulating the adaptation of metabolism during the peripartum period. Homeoresis represents the functioning of the endocrine system and metabolism in conditions when the organism must primarily provide certain physiological processes, such as fetal growth or lactation. Then the function of all tissues is adjusted to the new situation. Homeoretic hormones (growth hormone, prolactin, glucocorticosteroids, thyroid hormones, insulin, glucagon and leptin) in dairy cows in the peripartum period play a key role in maintaining high lactation and maintaining cow health.
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Звіти організацій з теми "Insulin metabolism"

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Gao, Hui, Chen Gong, Shi-chun Shen, Jia-ying Zhao, Dou-dou Xu, Fang-biao Tao, Yang Wang, and Xiao-chen Fan. A systematic review on the associations between prenatal phthalate exposure and childhood glycolipid metabolism and blood pressure: evidence from epidemiological studies. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, June 2022. http://dx.doi.org/10.37766/inplasy2022.6.0111.

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Review question / Objective: The present systematic review was performed to obtain a summary of epidemiological evidence on the relationships of in utero exposure to phthalates with childhood glycolipid metabolism and blood pressure. Condition being studied: Childhood cardiovascular risk factors including blood pressure, lipid profile (e.g., triglycerides, total cholesterol, HDL−C, LDL−C) and glucose metabolism (e.g., insulin, insulin resistance, insulin sensitivity, glucose) were the interested outcomes. Eligibility criteria: In brief, epidemiological studies including cohort study, case-control study and cross-sectional survey were screened. Studies regarding relationships between human exposure to organophosphate esters and neurotoxicity were possible eligible for the present systematic review. The adverse neurodevelopmental outcomes included development of cognition, behavior, motor, brain change, emotion, etc. Studies that did not meet the above criteria were not included in this systematic review.
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Research, Gratis. Brown Fat Activation: A Future Treatment for Obesity & Diabetes. Gratis Research, November 2020. http://dx.doi.org/10.47496/gr.blog.01.

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Brown fat holds a promising therapeutic approach to prevent obesity and type 2 diabetes by its profound effects on body weight reduction, heat generation, increased insulin sensitivity and glucose metabolism regulation
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Boisclair, Yves R., and Arieh Gertler. Development and Use of Leptin Receptor Antagonists to Increase Appetite and Adaptive Metabolism in Ruminants. United States Department of Agriculture, January 2012. http://dx.doi.org/10.32747/2012.7697120.bard.

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Objectives The original project had 2 major objectives: (1) To determine the effects of centrally administered leptin antagonist on appetite and adaptive metabolism in the sheep; (2) To develop and prepare second-generation leptin antagonists combining high binding affinity and prolonged in vivo half-life. Background Periods of suboptimal nutrition or exaggerated metabolic activity demands lead to a state of chronic energy insufficiency. Ruminants remain productive for a surprisingly long period of time under these circumstances by evoking adaptations sparing available energy and nutrients. The mechanism driving these adaptations in ruminant remains unknown, but could involve a reduction in plasma leptin, a hormone acting predominantly in the brain. In laboratory animals, reduced leptin signaling promotes survival during nutritional insufficiency by triggering energy sparing adaptations such as reduced thyroid hormone production and insulin resistance. Our overall hypothesis is that similar adaptations are triggered by reduced leptin signaling in the brain of ruminants. Testing of this hypothesis in ruminants has not been possible due to inability to block the actions of endogenous leptin and access to ruminant models where leptin antagonistic therapy is feasible and effective. Major achievements and conclusions The Israeli team had previously mutated 3 residues in ovine leptin, with no effect on receptor binding. This mutant was renamed ovine leptin antagonist (OLA) because it cannot activate signaling and therefore antagonizes the ability of wild type leptin to activate its receptor. To transform OLA into an effective in vivo antagonist, the Israeli made 2 important technical advances. First, it incorporated an additional mutation into OLA, increasing its binding affinity and thus transforming it into a super ovine leptin antagonist (SOLA). Second, the Israeli team developed a method whereby polyethylene glycol is covalently attached to SOLA (PEG-SOLA) with the goal of extending its half-life in vivo. The US team used OLA and PEG-SOLA in 2 separate animal models. First, OLA was chronically administered directly into the brain of mature sheep via a cannula implanted into the 3rdcerebroventricule. Unexpectedly, OLA had no effect of voluntary feed intake or various indicators of peripheral insulin action but reduced the plasma concentration of thyroid hormones. Second, the US team tested the effect of peripheral PEG-SOLA administration in an energy sensitive, rapidly growing lamb model. PEG-SOLA was administered for 14 consecutive days after birth or for 5 consecutive days before sacrifice on day 40 of life. Plasma PEG-SOLA had a half-life of over 16 h and circulated in 225- to 288-fold excess over endogenous leptin. PEG-SOLA administration reduced plasma thyroid hormones and resulted in a higher fat content in the carcass at slaughter, but had no effects on feed intake, body weight, plasma glucose or insulin. These results show that the team succeeded in developing a leptin antagonist with a long in vivo half-life. Moreover, in vivo results show that reduced leptin signaling promotes energy sparing in ruminants by repressing thyroid hormone production. Scientific and agricultural implications The physiological role of leptin in ruminants has been difficult to resolve because peripheral administration of wild type leptin causes little effects. Our work with leptin antagonists show for the first time in ruminants that reduced leptin signaling induces energy sparing mechanisms involving thyroid hormone production with little effect on peripheral insulin action. Additional work is needed to develop even more potent leptin antagonists, to establish optimal administration protocols and to narrow down phases of the ruminant life cycle when their use will improve productivity.
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Lekhanya, Portia Keabetswe, and Kabelo Mokgalaboni. Exploring the effectiveness of vitamin B12 complex and alpha-lipoic acid as a treatment for diabetic neuropathy. Protocol for systematic review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2022. http://dx.doi.org/10.37766/inplasy2022.5.0167.

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Review question / Objective: Does Alpha-Lipoic acid increase the uptake of glucose for better glycaemic control? Does vitamin B12 and Alpha-Lipoic acid improve inflammation? The aim of the study is to explore the effectiveness of Vitamin B12 and Alpha-Lipoic Acid as a possible treatment for diabetic neuropathy with major emphasis on markers of inflammation and glucose metabolism. Condition being studied: Diabetic Neuropathy (DN) is a heterogeneous type of nerve damage associated with diabetes mellitus, the condition most often damages nerves in the legs and feet. It presents both clinically and sub-clinically affecting the peripheral nervous system as a result of an increase in glucose concentration which interferes with nerve signalling. After the discovery of insulin as a treatment for Diabetes Mellitus (DM), the prevalence of DN has since increased significantly due to DM patients having a longer life expectancy. It has been estimated that atleast 50% of DM patients will develop DN in their life, with approximately 20% of these patients experiencing neuropathic pain. Nerves are susceptible to changes in glucose concentrations and insulin makes it impossible for neurons to continue regulating glucose uptake.
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yu, luyou, jinping yang, xi meng, and yanhua lin. Effectiveness of the gut microbiota-bile acid pathway (BAS) in the treatment of Type 2 diabetes: A protocol for systematic review and meta analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, July 2022. http://dx.doi.org/10.37766/inplasy2022.7.0117.

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Review question / Objective: To systematically evaluate the efficacy of the intestinal microbiome - bile acid pathway (BAS) in the treatment of T2DM. Condition being studied: Bile acids (BAs), an important component of bile, are also metabolites derived from cholesterol and promote intestinal absorption and transportation of dietary lipids . Studies have shown that bile acid receptor agonists can promote glP-1 secretion and improve glucose metabolism in preclinical mouse models of obesity and insulin resistance , which may become a new therapeutic target for Type 2 diabetes. However, no systematic review and meta-analysis has been found on the treatment of type 2 diabetes by intestinal microbiome - bile acid pathway. Therefore, we conducted a systematic review and meta-analysis to evaluate the safety and effectiveness of intestinal microbiome-bile acid pathway in the treatment of type 2 diabetes.
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Meidan, Rina, and Robert Milvae. Regulation of Bovine Corpus Luteum Function. United States Department of Agriculture, March 1995. http://dx.doi.org/10.32747/1995.7604935.bard.

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The main goal of this research plan was to elucidate regulatory mechanisms controlling the development, function of the bovine corpus luteum (CL). The CL contains two different sterodigenic cell types and therefore it was necessary to obtain pure cell population. A system was developed in which granulosa and theca interna cells, isolated from a preovulatory follicle, acquired characteristics typical of large (LL) and small (SL) luteal cells, respectively, as judged by several biochemical and morphological criteria. Experiments were conducted to determine the effects of granulosa cells removal on subsequent CL function, the results obtained support the concept that granulosa cells make a substaintial contribution to the output of progesterone by the cyclic CL but may have a limited role in determining the functional lifespan of the CL. This experimental model was also used to better understand the contribution of follicular granulosa cells to subsequent luteal SCC mRNA expression. The mitochondrial cytochrome side-chain cleavage enzyme (SCC), which converts cholesterol to pregnenolone, is the first and rate-limiting enzyme of the steroidogenic pathway. Experiments were conducted to characterize the gene expression of P450scc in bovine CL. Levels of P450scc mRNA were higher during mid-luteal phase than in either the early or late luteal phases. PGF 2a injection decreased luteal P450scc mRNA in a time-dependent manner; levels were significantly reduced by 2h after treatment. CLs obtained from heifers on day 8 of the estrous cycle which had granulosa cells removed had a 45% reduction in the levels of mRNA for SCC enzymes as well as a 78% reduction in the numbers of LL cells. To characterize SCC expression in each steroidogenic cell type we utilized pure cell populations. Upon luteinization, LL expressed 2-3 fold higher amounts of both SCC enzymes mRNAs than SL. Moreover, eight days after stimulant removal, LL retained their P4 production capacity, expressed P450scc mRNA and contained this protein. In our attempts to establish the in vitro luteinization model, we had to select the prevulatory and pre-gonadotropin surge follicles. The ratio of estradiol:P4 which is often used was unreliable since P4 levels are high in atretic follicles and also in preovulatory post-gonadotropin follicles. We have therefore examined whether oxytocin (OT) levels in follicular fluids could enhance our ability to correctly and easily define follicular status. Based on E2 and OT concentrations in follicular fluids we could more accurately identify follicles that are preovulatory and post gonadotropin surge. Next we studied OT biosynthesis in granulosa cells, cells which were incubated with forskolin contained stores of the precursor indicating that forskolin (which mimics gonadotropin action) is an effective stimulator of OT biosynthesis and release. While studying in vitro luteinization, we noticed that IGF-I induced effects were not identical to those induced by insulin despite the fact that megadoses of insulin were used. This was the first indication that the cells may secrete IGF binding protein(s) which regonize IGFs and not insulin. In a detailed study involving several techniques, we characterized the species of IGF binding proteins secreted by luteal cells. The effects of exogenous polyunsaturated fatty acids and arachidonic acid on the production of P4 and prostanoids by dispersed bovine luteal cells was examined. The addition of eicosapentaenoic acid and arachidonic acid resulted in a dose-dependent reduction in basal and LH-stimulated biosynthesis of P4 and PGI2 and an increase in production of PGF 2a and 5-HETE production. Indomethacin, an inhibitor of arachidonic acid metabolism via the production of 5-HETE was unaffected. Results of these experiments suggest that the inhibitory effect of arachidonic acid on the biosynthesis of luteal P4 is due to either a direct action of arachidonic acid, or its conversion to 5-HETE via the lipoxgenase pathway of metabolism. The detailed and important information gained by the two labs elucidated the mode of action of factors crucially important to the function of the bovine CL. The data indicate that follicular granulosa cells make a major contribution to numbers of large luteal cells, OT and basal P4 production, as well as the content of cytochrome P450 scc. Granulosa-derived large luteal cells have distinct features: when luteinized, the cell no longer possesses LH receptors, its cAMP response is diminished yet P4 synthesis is sustained. This may imply that maintenance of P4 (even in the absence of a Luteotropic signal) during critical periods such as pregnancy recognition, is dependent on the proper luteinization and function of the large luteal cell.
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McGuire, Mark A., Amichai Arieli, Israel Bruckental, and Dale E. Bauman. Increasing Mammary Protein Synthesis through Endocrine and Nutritional Signals. United States Department of Agriculture, January 2001. http://dx.doi.org/10.32747/2001.7574338.bard.

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Objectives To determine endocrine factors that regulate the partitioning of amino acids by the mammary gland. To evaluate dietary flow and supply of energy and amino acids and their effects on milk protein synthesis and endocrine status. To use primary cultures of cow mammary epithelial cells to examine the role of specific factors on the rates and pattern of milk protein synthesis. Milk protein is an increasingly valuable component of milk but little is known regarding the specific hormonal and nutritional factors controlling milk protein synthesis. The research conducted for this project has determined that milk protein synthesis has the potential to be enhanced much greater than previously believed. Increases of over 25% in milk protein percent and yield were detected in studies utilizing abomasal infusion of casein and a hyperinsulinemic-euglycemic clamp. Thus, it appears that insulin, either directly or indirectly, can elicit a substantial increase in milk protein synthesis if additional amino acids are supplied. For additional amino acids, casein provided the best response even though substantial decreases in branched chain amino acids occur when the insulin clamp is utilized. Branched chain amino acids alone are incapable of supporting the enhanced milk protein output. The mammary gland can vary both blood flow and extraction efficiency of amino acids to support protein synthesis. A mammary culture system was used to demonstrate specific endocrine effects on milk protein synthesis. Insulin-like growth factor-I when substituted for insulin was able to enhance casein and a-lactalbumin mRNA. This suggests that insulin is a indirect regulator of milk protein synthesis working through the IGF system to control mammary production of casein and a-lactalbumin. Principal component analysis determined that carbohydrate had the greatest effect on milk protein yield with protein supply only having minor effects. Work in cattle determined that the site of digestion of starch did not affect milk composition alone but the degradability of starch and protein in the rumen can interact to alter milk yield. Cows fed diets with a high degree of rumen undegradability failed to specifically enhance milk protein but produced greater milk yield with similar composition. The mammary gland has an amazing ability to produce protein of great value. Research conducted here has demonstrated the unprecedented potential of the metabolic machinery in the mammary gland. Insulin, probably signaling the mammary gland through the IGF system is a key regulator that must be combined with adequate nutrition in order for maximum response.
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Butler, Walter R., Uzi Moallem, Amichai Arieli, Robert O. Gilbert, and David Sklan. Peripartum dietary supplementation to enhance fertility in high yielding dairy cows. United States Department of Agriculture, April 2007. http://dx.doi.org/10.32747/2007.7587723.bard.

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Анотація:
Objectives of the project: To evaluate the effects of a glucogenic supplement during the peripartum transition period on insulin, hepatic triglyceride accumulation, interval to first ovulation, and progesterone profile in dairy cows. To compare benefits of supplemental fats differing in fatty acid composition and fed prepartum on hepatic triglyceride accumulation, interval to first ovulation, progesterone profile, and uterine prostaglandin production in lactating dairy cows. To assess the differential and carry-over effects of glucogenic and fat supplements fed to peripartum dairy cows on steroidogenesis and fatty acids in ovarian follicles. To determine the carry-over effects of peripartum glucogenic or fat supplements on fertility in high producing dairy cows (modified in year 3 to Israel only). Added during year 3 of project: To assess the activity of genes related to hepatic lipid oxidation and gluconeogenesis following dietary supplementation (USA only). Background: High milk yields in dairy cattle are generally associated with poor reproductive performance. Low fertility results from negative energy balance (NEBAL) of early lactation that delays resumption of ovarian cycles and exerts other carryover effects. During NEBAL, ovulation of ovarian follicles is compromised by low availability of insulin and insulin-like growth factor-I (IGF-I), but fatty acid mobilization from body stores is augmented. Liver function during NEBAL is linked to the resumption of ovulation and fertility: 1) Accumulation of fatty acids by the liver and ketone production are associated with delayed first ovulation; 2) The liver is the main source of IGF-I. NEBAL will continue as a consequence of high milk yield, but dietary supplements are currently available to circumvent the effects on liver function. For this project, supplementation was begun prepartum prior to NEBAL in an effort to reduce detrimental effects on liver and ovarian function. Fats either high or low in unsaturated fatty acids were compared for their ability to reduce liver triglyceride accumulation. Secondarily, feeding specific fats during a period of high lipid turnover caused by NEBAL provides a novel approach for manipulating phospholipid pools in tissues including ovary and uterus. Increased insulin from propylene glycol (glucogenic) was anticipated to reduce lipolysis and increase IGF-I. The same supplements were utilized in both the USA and Israel, to compare effects across different diets and environments. Conclusions: High milk production and very good postpartum health was achieved by dietary supplementation. Peripartum PGLY supplementation had no significant effects on reproductive variables. Prepartum fat supplementation either did not improve metabolic profile and ovarian and uterine responses in early lactation (USA) or decreased intake when added to dry cow diets (Israel). Steroid production in ovarian follicles was greater in lactating dairy cows receiving supplemental fat (unsaturated), although in a field trail fertility to insemination was not improved.
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