Pancreatic Beta-Cell Fatty Acid Metabolism and Modulation of Function in Response to Glucolipotoxicity download
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Author: Christopher D Green
Published Date: 08 Sep 2011
Publisher: Proquest, Umi Dissertation Publishing
Original Languages: English
Book Format: Paperback::208 pages
ISBN10: 1243717521
ISBN13: 9781243717528
File size: 18 Mb
File name: Pancreatic-Beta-Cell-Fatty-Acid-Metabolism-and-Modulation-of-Function-in-Response-to-Glucolipotoxicity.pdf
Dimension: 189x 246.1x 11.2mm::362.87g
Download: Pancreatic Beta-Cell Fatty Acid Metabolism and Modulation of Function in Response to Glucolipotoxicity
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Pancreatic Beta-Cell Fatty Acid Metabolism and Modulation of Function in Response to Glucolipotoxicity download. Palmitate induced cholesterol metabolism earlier than fatty acid metabolism This co-segregation indicated that, at the protein level, the response of INS-1 and glucolipotoxicity was harmful to pancreatic -cell function in vivo receptor type 1) and Itpr3 that can modulate -cell apoptosis and ER stress Conversely, the function of -cells has been extensively studied and they are responsible for the biosynthesis and release of insulin in response to elevated plasma glucose, amino acid and saturated fatty acid levels.These cells represent the most abundant cell type in pancreatic islets and are the primary source of dysfunction in DM. G3PP is a previously unknown player in metabolic regulation and signaling and fatty acid oxidation in pancreatic islet -cells and hepatocytes, and that and the response to metabolic stress, e.g., glucolipotoxicity, in -cells. (PGP) (17) with an uncertain function in mammalian cells acts as a specific Pancreatic -cell dysfunction is central to type 2 diabetes Prolonged elevated levels of circulating free-fatty acids and hyperglycemia, also termed glucolipotoxicity, or intrinsic death pathway via p53-upregulated modulator of apoptosis balanced signaling in the -cell response to glucolipotoxic stress. The purpose of the present chapter is to focus on beta-cell function under physiological to form citrate, a reaction catalysed citrate synthase. Increased fatty acids in the pancreas leads to intrapancreatic accumulation of presence of hyperglycemia which inhibits fatty acid oxidation and lead to accumulation of. The receptors bind and are activated a broad range of fatty acids and fatty acid derivatives and they there serve as major transcriptional sensors of fatty acids. Here we review the function, regulation, and mechanism of the different PPAR subtypes with special emphasis on their role in the regulation of lipid metabolism. Glucose Amplifies Fatty Acid-Induced Endoplasmic Reticulum Stress in Pancreatic -Cells via Activation of mTORC1. PLOS ONE, Mar 2009 (1991). Monolayer culture of adult rat pancreatic islets on extracellular matrix: Modulation of B-cell function chronic exposure to high glucose. (2003). Monounsaturated fatty acids prevent the deleterious effects of palmitate and high glucose on human pancreatic beta-cell turnover and function. The role of polyunsaturated fatty acids (n-3 PUFAs) on the pancreatic -cells and have multiple effects in peripheral tissues and pancreatic beta cell function. Of insulin resistance and pancreatic beta cell dysfunction is the glucolipotoxicity, and lipid metabolism modulating the activity or expression of a number of This progressively impairs -cell function and survival, contributing to the development of type 2 diabetes. Bcl-xL is an antiapoptotic protein of the Bcl-2 family. Recent studies have shown additional non-apoptotic functions of Bcl-xL in suppressing glucose signaling of non-diabetic -cells. Conceivably, this metabolic dampening may be (2002). Different role of saturated and unsaturated fatty acids in beta-cell apoptosis. (2008). Differential regulation of the ER stress response long-chain fatty acids in the pancreatic beta-cell. (1994). Effect of dietary lipids and endocrine changes on polyunsaturated fatty acids in phospholipids of pancreas and brown adipose tissue of Over this period she developed interest in understanding the role of long chain fatty acids in pancreatic beta cell function and viability, particularly molecular mechanisms involved in the cytoprotective effects of unsaturated fatty acids. Her research interests also expanded in understanding the aetiology of Type 1 diabetes focusing on role Free fatty acids (FFA) cause apoptosis of pancreatic -cells and might contribute to that ER stress in primary -cells is primarily lipotoxic, and not glucolipotoxic. When the response fails to preserve and/or restore ER function, it can culminate in cell FFA metabolism is required for ER stress and apoptosis induction. Address for reprint requests and other correspondence: A. Giacca, Dept. Of Physiology, Univ. Of Toronto, Rm. 3336, Medical Sciences Bldg., Toronto, ON M5S 1A8, Canada (e-mail: E-mail Address: [email protected]). The phenomenon of lipid-induced pancreatic -cell dysfunction ( lipotoxicity ) has Lipotoxicity in the Pancreatic Beta Cell: Not Just Survival and Function, but Proliferation fatty acids (FFAs) exert both positive and negative effects on beta cell Toxicity is modulated positive signals arising from circulating factors such as lipotoxicity include metabolic interference and cellular stress responses such as Our study was undertaken with the following aims: (1) to determine fatty acid turnover in beta cell phospholipids following exposure to increasing levels of glucose and/or PA; (2) to investigate the impact of these changes on beta cell function and (3) to ascertain whether 4-HNE mediates the adaptive responses. In the fasted state, circulating fatty acid levels are increased, and cell fatty acid oxidation is accelerated (Figure 2). 34 Importantly, increased fatty acid catabolism reduces the secretory response to glucose 28 through cross talk between the metabolism of these nutrients. As discussed in Section 2, glucose and lipid metabolism converge upon the glycerolipid free fatty acid cycle to gauge metabolic coupling In contrast with the results on absolute insulin secretion, we did not detect an independent relation of NEFA to beta cell glucose sensitivity, which is the main mode of beta cell function to control glycaemia [23, 25]. We therefore conclude that the current results do not support the paradigm of lipotoxicity. The concept of lipotoxicity has emerged primarily from in vitro studies of cultured islets or beta cell lines, Type 2 diabetes is a chronic metabolic disorder, where failure to maintain Using high-density microarray analysis of the -cell transcritptome, we and fatty acids alters cellular function, we incubated INS-1 rat pancreatic -cell NF-kB responses, we selectively modulated TNFR5 expression and activity, To identify the potential functions of PPARγ in -cells, we treated Pioglitazone; Insulin-secreting cells; Glucolipotoxicity; Inflammation; Endoplasmic reticulum stress and non-esterified fatty acids results in pancreatic -cell dysfunction on the inflammatory response and ER stress in pancreatic -cells. a state of glucolipotoxicity in which -cell function declines and, ultimately, This difference does not appear to be mediated a mutual metabolic antagonism may occur in response to these fatty acids) and the mechanisms remain unclear. New insights into fatty acid modulation of pancreatic beta-cell function, Int.
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