Metabolic Effects Of Glucagon In Endogenous Hypertriglyceridemia

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The Antidiabetogenic Effect of GLP-1 Is Maintained During a 7

12 and 14, suggesting that there was not enough GLP-1 left to stimulate endogenous insulin release and compensate for the decrease in the dose of exogenous insulin. Therefore, the effect

Free Fatty Acid Receptors FFAR1 and GPR120 as Novel

ported to contribute to the secretion of glucagon-like peptide-1 (GLP-1), adipocyte differentiation, and anti-inflammatory effects.13,14 Thus, these physio-logical functions are considered to be involved in metabolic disorders such as type 2 diabetes. There-fore, FFARs have received considerable attention as

Oxandrolone Treatment in Adults with Severe Thermal Injury

Oxandrolone Treatment in Adults with Severe Thermal Injury JamesT.Miller,Pharm.D.,andImadF.Btaiche,Pharm.D. Severethermalinjuryisassociatedwithhypermetabolismandhyper-

Soluble (pro)renin receptor treats metabolic syndrome in mice

insulin, dipeptidyl peptidase-4, and glucagon-like peptide-1, are used only for glycemic control and have little benefit for other components of metabolic syndrome (4). Moreover, these therapies are often associated with adverse effects, for example, one class of highly effective antidiabetic drugs, thiazolidinediones (TZDs),

The metabolic syndrome: A tug-of-war with no winner

Effects on fat and protein metabolism Two counterregulatory hormones, growth hormone and glucocorticoids, have differ-ent effects on lipid and protein metabolism that may be important in the development and maintenance of the metabolic syn-drome. Growth hormonelevels are often low in the metabolic syndrome,3 and this counter-

Could TDX-1 explain the changes observed in endocrine

Nov 20, 2020 pancreatic storage of insulin and glucagon and produces some alterations related to metabolic syndrome (hyperglycemia and hypertriglyceridemia) with an increase in oxidative stress [10 13]. Moreover, we also demonstrated that consumption of cola beverages, regardless sugar content,

Hepatic lipid accumulation: cause and consequence of

independent of origin, promotes systemic metabolic dysfunction. The severity of fatty liver disease is directly related to classic components of the metabolic syndrome including central obesity, insulin resistance, hyperinsulinemia, hypertriglyceridemia and hyperglycemia (Bedogni et al. 2005, Wainwright & Byrne 2016). In fact, 60 70% of

Biochimica et Biophysica Acta - COnnecting REpositories

major metabolic hormones such as insulin, glucagon, leptin and IGF1. The striking metabolic phenotype in FGF19 overexpressing animals can be partly explained by changes in liver gene expression. In the Biochimica et Biophysica Acta 1812 (2011) 791 795 ⁎ Corresponding author. Tel.: +1 3172760091; fax: +1 3172769574.

INSULIN STIMULATION OF STEROL REGULATORY ELEMENT-BINDING

Glucagon is a peptide hormone produced in alpha cells of the islets of Langerhans that acts in opposition to insulin. Glucagon is secreted from the pancreas in response to low blood glucose, acting as a signal for nutritional deficit. Systemic effects of glucagon include glycogen breakdown (glycogenolysis), fatty acid oxidation, and

IL-6: A Potential Role in Cardiac Metabolic Homeostasis

Cardiac metabolic features and consequences of myocardial lipotoxicity are also briefly analyzed. Finally, the roles of IL-6 in cardiac FA uptake (i.e., serum lipid profile and myocardial FA

Malnutrition, Infection, and Immune Function

states), or by the metabolic effects of infection. The consequence is impairment of host de-fenses, which in turn leads to an increased burden of infection and further malnutrition. (From ref. 12.) ciency in a single dietary component. Instead, it is a complex and variable mosaic of deficiency, adequacy, or even excess of different dietary

Pharmacological Modulators of Endoplasmic Reticulum Stress in

cellular damage from ER stress. Based on previous reports, we have reviewed the protective effects of various drugs against cell damage caused by ER stress. 2. Cellular Aspects of ER-Stress and Metabolic Diseases 2.1. Diabetes Mellitus Growing evidences support a critical role for activation of -cell ER stress pathways in pathophysiology of

Proefschrift Edwin Parlevliet 180810

Effects of CNTO736 treatment on insulin sensitivity 37 Introduction Glucagon-like peptide 1 (GLP-1) is an incretin hormone synthesized in enteroendocrine L-cells and brain tissue 1, 2. It is released by the gut in response to food intake to stimulate glucose-induced insulin production 1, 3. In addition, GLP-1 exerts multiple other effects,

Cannabinoid receptors are differentially regulated in the

biomarkers: glucose intolerance, hyperinsulinemia, insulin resistance, hypertriglyceridemia, and an increase in visceral adiposity. To determine the presence of CB1 and CB2 receptors in pancreatic β cells, immunofluorescence of primary cell cultures and pancreatic sections was performed. For

Metabolic effects of the incretin mimetic exenatide in the

incretin mimetics, which replicate several glucoregulatory effects of the endogenous incretin hormone, glucagon-like peptide-1 (GLP-1). Currently approved in the US as an injectable adjunct to metformin and/or sulfonylurea therapy, exenatide improves glycemic control through

Loyola University Chicago Loyola eCommons

THE METABOLIC RESPONSE TO NATURAL DIETS CONTAINING VARIABLE AMOUNTS OF SUCROSE IN HYPERTRIGLYCERIDEMIA PRONE DIABETICS Walter S. Jellish A Dissertation Submitted to the Faculty of the Graduate School of Loyola University of Chicago in Partial Fulfillment of the Requirements for the Degree of Doctor of Philosophy

Effects of Epeleuton, a Novel Synthetic Second‐Generation n‐3

lence of metabolic syndrome, type 2 diabetes mellitus, and dyslipidemia in patients with NAFLD,1 secondary and post hoc analyses were undertaken to compare the lipid-lowering, antihyperglycemic, and anti-inflam-matory effects of epeleuton 1 g/day and epeleuton 2 g/ day with placebo. On the basis of nonclinical pharma-

Rezulin® - Food and Drug Administration

hypertriglyceridemia characteristic of insulin-resistant states such as type 2 diabetes. Plasma lactate and ketone body formation are also decreased. The metabolic changes produced by troglitazone result from the increased responsiveness of insulin-dependent tissues and are observed in numerous animal models of insulin resistance.

Functional Characterization of the Semisynthetic Bile Acid

levels in conditions such as hypertriglyceridemia, metabolic syndrome, type 2 diabetes, nonalcoholic steatohepatitis, and obesity. Similar to effects in the liver, FXR agonists modulate lipid metabolism and promote anti-inflammatory and antifi-brotic effects in the kidney, suggesting a potential use of FXR

The Prevention & Treatment of Metabolic Syndrome in Primary Care

Metabolic Syndrome in Primary Care Common first choice due to lack of systemic side effects and long history 22 suppresses endogenous glucose production 3.

Session IV - CiteSeerX

endogenous humoral responses to injury and infection. Infusion of this protein is known to elicit an increase in circulating counterregulatory hormone levels, 22 and may also promote release of other monokines, including IL-l, and other lymphokines.23 Therefore, the hemodynamic and metabolic effects of cachectin/TNF in vivo are likely

ORIGINAL ARTICLE Lack of FFAR1/GPR40 Does Not Protect Mice

peutic targets for metabolic disease (2 4). Interest in FFAR1 intensified in 2005 when Steneberg et al. (5) reported that mice lacking FFAR1 were resistant to a number of the effects of a high-fat diet, including hyperinuslinemia, hyperglycemia, hypertriglyceridemia, and hepatic steatosis. Conversely, Steneberg et al. also

SUMMARY REVIEW - Food and Drug Administration

Exenatide (Byetta®) is a synthetically manufactured 34-amino acid glucagon-like peptide 1 (GLP-1) agonist that was originally isolated from the saliva of the Gila monster lizard. GLP-1 is an incretin hormone that increases insulin secretion in response to an ingested meal. Because human GLP-1 is

Glucagon II - gbv.de

D. Modulatory Effects of Glucose on A-cell Function 13 I. Acute Effects 13 II. Prolonged and Chronic Effects 13 References 15 CHAPTER 24 The Amino Acid-Induced Secretion of Glucagon R. ASSAN, M. MARRE, and M. GORMLEY. With 8 Figures A. Introduction 19 B. Phenomenology 19 I. In Vitro 19 1. Isolated Perfused Pancreas 19 2.

Fibroblast Growth Factor-21 as a Therapeutic Agent for

Important- ing FGF21 levels and resulted in serious metabolic abnormalities, ly, these effects were not associated only with the HFHC diet, assuch as fatty liver, severe hypertriglyceridemia

Pharmacological Sciences 2005; 9: 191-208 Postprandial

metabolic syndrome should be also controlled to decrease the risk of cardiovascular disease and the consequent mortality. Table I summarizes some of the changes induced by postprandial hyperglycemia and hypertriglyceridemia on the homeostatic mechanisms of different organs and tissues8,24. Some of these effects were also observed in non

Insulin Clearance After Oral and Intravenous Glucose

The greater effect of RYGB on metabolic improvements is often confounded by greater weight loss post-RYGB (10). Some of the superior effects of RYGB and VSG compared with diet or AGB on post-prandial glucose are thought to be me-diated by increased postprandial levels of GLP-1 (11,12). It remains unclear what role incretins may play in hepatic ICR,

Cell Metabolism Article

obesity, hypertriglyceridemia, low high-density lipoprotein cholesterol (HDL-C) levels, and hypertension (Moller and Kauf-man, 2005). A limitation of currently available drug classes for the treatment of risk factors associated with the metabolic syn-drome is that no single agent (e.g., statin, fibrate, or metformin)

University of Groningen Altered lipid and bile acid

of GSD Ia to selectively establish effects of increased intrahepatic glucose sensing on several metabolic processes in the liver. Importantly, GSD Ia provides a model for diabetic liver disease (1,2), a major global health problem. Although deviations in blood glucose are opposite in GSD Ia and type 2 diabetes (low high versus

The metabolic syndrome: A tug-of-war with no winner

The metabolic syndrome: glucagon, and catecholamines, along with free PHYSIOLOGIC EFFECTS Dyslipidemia Visceral obesity High blood pressure Increased resting heart rate

Incretins and selective renal sodium-glucose co-transporter 2

In animal models, stable analogues of glucagon-like peptide-1 (GLP-1) were able to reduce body weight and blood pressure and also had favorable effects on ischemia following coronary reperfusion. In a similar way, dipeptidyl peptidase IV (DPP-IV) showed to have favorable effects in animal models of ischemia/ reperfusion.

Intracerebroventricular Neuropeptide Y Infusion Precludes

suppression of endogenous glucose and VLDL pro-duction in response to food intake. Accordingly, the metabolic features of obesity and type 2 diabetes include hyperglycemia and hypertriglyceridemia. It was shown recently that hypothalamic insulin signal-ing is required for inhibition of endogenous glucose pro-duction (EGP) (3).

The Acute Metabolic Effects of Tumor Necrosis Factor

endogenous host-produced factors synthesized as a part of the host immunologie response to invasive tumor growth may contribute to the metabolic abnormalities ofcachexia. Several lines of investigation have implicated the macro¬ phage as the source of such factors. Mononuclear phago¬ cytes are known infiltrate tumors in vivo, and on

Markedly Blunted Metabolic Effects of Fructose in Healthy

ated with adverse metabolic effects (1). Few studies have addressed whether the metabolic effects of fructose are sex dependent, however. In rats, sev-eral reports show that fructose has more pronounced adverse metabolic effects in males than in females (2,3); similarly, in humans, only men showed fructose-induced hypertriglyceridemia (4,5). The

CNTO736, a Novel GLP-1 Receptor Agonist, Ameliorates Insulin

Oct 10, 2008 Glucagon-like peptide 1 (GLP-1) is an incretin hormone synthesized in enteroendocrine L- cells and brain tissue (Kreymann, et al., 1987;Larsen, et al., 1997). It is released by the gut in

Distinct but complementary contributions of PPAR isotypes to

metabolic diseases such as type 2 diabetes and non-alcoholic fatty liver disease. While they share anti-inflammatory activities, the PPAR isotypes distinguish themselves by differential actions on lipid and glucose homeostasis. In this Review we discuss the complementary and distinct metabolic effects of the PPAR isotypes together with the

FGF21: A novel prospect for the treatment of metabolic

FGF21 in the treatment of metabolic diseases Kharitonenkov & Shanafelt 361 such as β-hydroxybutyrate, as well as in the development of fatty liver, hypertriglyceridemia and insulin resistance, and

Glycogen storage diseases: New perspectives

Glycogen storage diseases (GSD) are inherited metabolic disorders of glycogen metabolism (Figure 1)[1,2]. In postprandial period, blood glucose level increases and endogenous glucose production is suppressed. Exogenous glucose is either metabolized to pyruvate or stored as glycogen in the liver and skeletal muscle[1]. Under aerobic

Pantethine: A Review of its Biochemistry and Therapeutic

zymes. In experimental models, glucagon in-creases, while insulin decreases, the incorpo-ration of pantothenic acid into CoA. Gluco-corticoids appear to potentiate the effects of glucagon.3 Hyperthyroidism is also reported to increase CoA synthesis. 4 Metabolism of Pantethine The metabolic fate of an oral dose of

RESEARCH ARTICLE Open Access Localization of lipoprotein

in metabolic processes [1,2]. LPL is synthesized and secreted by parenchymal cells such as adipocytes and myocytes, but the enzyme acts at the luminal face of endothelial cells in capillaries where it is anchored to the plasma membrane in a heparin-releasable manner. The mechanism by which LPL is transported from