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Fatty acids and beta-cell function

Published on Mar 1, 1997in Diabetologia 7.11
· DOI :10.1007/BF03168182
A. Björklund3
Estimated H-index: 3
(KI: Karolinska Institutet),
G. Yaney1
Estimated H-index: 1
(BMC: Boston Medical Center)
+ 1 AuthorsGordon C. Weir83
Estimated H-index: 83
(Joslin Diabetes Center)
Cite
Abstract
at the Third JDF World Conference on Diabetes Research held in Monaco in 1991 there was little, if any, mention of the role of fatty acids in pancreatic betacell function. However, this situation has now changed dramatically on the heels of two recent and simultaneousdevelopments. The first has to do with the notion that there is at work within the beta cell, just as in other tissues, an important element of glucose-fatty acid “cross-talk” which appears to be essential for the normal regulation of insulin secretion. The second revelation is that chronic exposureof the beta cell to high levels of circulating fatty acids can actually be detrimental tostimulus-secretioncoupling,andmightbeafactor intheaetiologyofnon-insulin-dependent,andpossibly insulin-dependent, diabetes. Thus, the emerging pictureisthatfromthestandpointofbeta-cell functionfatty acidscan play“a good,a badandanugly”role.These characteristics form the subject of the current session.
  • References (14)
  • Citations (14)
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References14
Newest
Published on Jul 15, 1997in Journal of Clinical Investigation 12.28
Daniel T. Stein23
Estimated H-index: 23
(UTSW: University of Texas Southwestern Medical Center),
B E Stevenson3
Estimated H-index: 3
(UTSW: University of Texas Southwestern Medical Center)
+ 4 AuthorsJ. D. McGarry48
Estimated H-index: 48
(UTSW: University of Texas Southwestern Medical Center)
Lowering of the elevated plasma FFA concentration in 18- 24-h fasted rats with nicotinic acid (NA) caused complete ablation of subsequent glucose-stimulated insulin secretion (GSIS). Although the effect of NA was reversed when the fasting level of total FFA was maintained by coinfusion of soybean oil or lard oil (plus heparin), the more saturated animal fat proved to be far more potent in enhancing GSIS. We therefore examined the influence of individual fatty acids on insulin secretion in the pe...
Published on Mar 1, 1997in Diabetes 7.20
Thierry Brun21
Estimated H-index: 21
,
Françhise Assimacopoulos-Jeannet1
Estimated H-index: 1
+ 1 AuthorsMarc Prentki67
Estimated H-index: 67
The mechanism whereby long-term exposure of the β-cell to fatty acids alters the β-cell response to glucose is not known. We hypothesized that fatty acids may alter β-cell function by changing the expression level of metabolic enzymes implicated in the regulation of insulin secretion, in particular acetyl-CoA carboxylase (ACC). This enzyme catalyzes the formation of malonyl-CoA, a key regulator of fatty acid oxidation. Using the β-cell line INS-1 as a model, the results show that the polyunsatur...
Published on Jan 31, 1997in Journal of Biological Chemistry
Enrique Roche25
Estimated H-index: 25
(UdeM: Université de Montréal),
Françoise Assimacopoulos-Jeannet1
Estimated H-index: 1
(University of Geneva)
+ 5 AuthorsMarc Prentki67
Estimated H-index: 67
(UdeM: Université de Montréal)
Abstract Chronic elevation in glucose has pleiotropic effects on the pancreatic β-cell including a high rate of insulin secretion at low glucose, β-cell hypertrophy, and hyperplasia. These actions of glucose are expected to be associated with the modulation of the expression of a number of glucose-regulated genes that need to be identified. To further investigate the molecular mechanisms implicated in these adaptation processes to hyperglycemia, we have studied the regulation of genes encoding k...
Published on Jan 17, 1997in Journal of Biological Chemistry
F. Assimacopoulos-Jeannet33
Estimated H-index: 33
(University of Geneva),
Stéphane Thumelin4
Estimated H-index: 4
(UdeM: Université de Montréal)
+ 3 AuthorsMarc Prentki67
Estimated H-index: 67
(UdeM: Université de Montréal)
Abstract Fatty acids are important metabolic substrates for the pancreatic β-cell, and long term exposure of pancreatic islets to elevated concentrations of fatty acids results in an alteration of glucose-induced insulin secretion. Previous work suggested that exaggerated fatty acid oxidation may be implicated in this process by a mechanism requiring changes in metabolic enzyme expression. We have therefore studied the regulation of carnitine palmitoyltransferase I (CPT I) gene expression by fat...
B. A. Cunningham1
Estimated H-index: 1
(BU: Boston University),
Jude T. Deeney23
Estimated H-index: 23
(BU: Boston University)
+ 2 AuthorsKeith Tornheim24
Estimated H-index: 24
(BU: Boston University)
Normal insulin secretion is oscillatory in vivo and from groups of perifused islets. Stimulation of rat islets with different glucose concentrations gave insulin oscillations of similar period (5-8 min) but increasing amplitude. It has been assumed that oscillatory secretion is due to oscillations in intracellular free Ca2+, as seen in single islets and single pancreatic beta-cells. However, when islets were perifused with diazoxide and high KCl to maintain high intracellular free Ca2+, insulin ...
Published on Jun 15, 1996in Journal of Clinical Investigation 12.28
Daniel T. Stein23
Estimated H-index: 23
(UTSW: University of Texas Southwestern Medical Center),
Victoria Esser27
Estimated H-index: 27
(UTSW: University of Texas Southwestern Medical Center)
+ 5 AuthorsJ. D. McGarry48
Estimated H-index: 48
(UTSW: University of Texas Southwestern Medical Center)
We asked whether the well known starvation-induced impairment of glucose-stimulated insulin secretion (GSIS) seen in isolated rat pancreas preparations also applies in vivo. Accordingly, fed and 18-24-h-fasted rats were subjected to an intravenous glucose challenge followed by a hyperglycemic clamp protocol, during which the plasma-insulin concentration was measured. Surprisingly, the acute (5 min) insulin response was equally robust in the two groups. However, after infusion of the antilipolyti...
Published on May 3, 1996in Journal of Biological Chemistry
Olof Larsson36
Estimated H-index: 36
(KI: Karolinska Institutet),
Jude T. Deeney8
Estimated H-index: 8
(KI: Karolinska Institutet)
+ 2 AuthorsBarbara E. Corkey56
Estimated H-index: 56
(BMC: Boston Medical Center)
Abstract Long term exposure to elevated levels of long chain free fatty acids decreases glucose-induced insulin secretion from pancreatic islets and clonal pancreatic β-cells. The mechanism for this loss of glucose sensitivity is at present not known. In this study, we evaluated the possibility that increases in long chain acyl-CoA esters (LC-CoA), the metabolically active form of free fatty acids, might mediate the loss of glucose sensitivity. We observed that cellular levels of LC-CoA increase...
Published on May 1, 1996in Diabetes 7.20
Yun-Ping Zhou6
Estimated H-index: 6
,
Per-Olof Berggren68
Estimated H-index: 68
,
Valdemar Grill46
Estimated H-index: 46
We studied the effects of fatty acid oxidation on insulin secretion of db/db mice and underlying molecular mechanisms of these effects. At 2–3 months of age, db/db mice were markedly obese, hyperglycemic, and hyperinsulinemic. Serum free fatty acid (FFA) levels were increased in 2-month-old (1.5 ± 0.1 vs. 1.1 ± 0.1 mmol/l, P P db /+ mice serving as controls. Glucose-induced insulin release from db/db islets was markedly decreased compared with that from db /+ islets and was specifically ameliora...
Published on May 1, 1996in Biochemical Journal 4.33
Vildan N. Civelek9
Estimated H-index: 9
,
Jude T. Deeney23
Estimated H-index: 23
+ 3 AuthorsBarbara E. Corkey56
Estimated H-index: 56
(BMC: Boston Medical Center)
Stimulation of insulin release by glucose requires increased metabolism of glucose and a rise in cytosolic free Ca 2+ in the pancreatic β-cell. It is accompanied by increases in respiratory rate, pyridine and flavin nucleotide reduction state, intracellular pH and the ATP/ADP ratio. To test alternative proposals of the regulatory relationships among free Ca 2+ , mitochondrial metabolism and cellular energy state, we determined the temporal sequence of these metabolic and ionic changes following ...
Published on Mar 1, 1996in Diabetes 7.20
Marc Prentki67
Estimated H-index: 67
,
Barbara E. Corkey56
Estimated H-index: 56
Widely held theories of the pathogenesis of obesity-associated NIDDM have implicated apparently incompatible events as seminal: 1 ) insulin resistance in muscle, 2 ) abnormal secretion of insulin, and 3 ) increases in intra-abdominal fat. Altered circulating or tissue lipids are characteristic features of obesity and NIDDM. The etiology of these defectss is not known. In this perspective, we propose that the same metabolic events, elevated malonyl-CoA and long-chain acyl-CoA (LC-CoA), in various...
Cited By14
Newest
Published on Sep 3, 2014in PLOS ONE 2.78
Simon G. Anderson26
Estimated H-index: 26
(University of Manchester),
Warwick B. Dunn50
Estimated H-index: 50
(University of Manchester)
+ 6 AuthorsJ. Kennedy Cruickshank29
Estimated H-index: 29
(University of Manchester)
Background: Blood-vessel dysfunction arises before overt hyperglycemia in type-2 diabetes (T2DM). We hypothesised that a metabolomic approach might identify metabolites/pathways perturbed in this pre-hyperglycemic phase. To test this hypothesis and for specific metabolite hypothesis generation, serum metabolic profiling was performed in young women at increased, intermediate and low risk of subsequent T2DM. Methods: Participants were stratified by glucose tolerance during a previous index pregna...
Published on Aug 1, 2011in Nutrition & Diabetes 3.10
Lara Nyman3
Estimated H-index: 3
(UAB: University of Alabama at Birmingham),
Liqun Tian11
Estimated H-index: 11
(UAB: University of Alabama at Birmingham)
+ 4 AuthorsP A Wood1
Estimated H-index: 1
(Sanford-Burnham Institute for Medical Research)
Long-term effects of high-fat or high-carbohydrate diets on glucose tolerance in mice with heterozygous carnitine palmitoyltransferase-1a deficiency
Published on Jul 12, 2011in Journal of Endocrinological Investigation
Salvatore Piro21
Estimated H-index: 21
(University of Catania),
Agata Maria Rabuazzo19
Estimated H-index: 19
(University of Catania)
+ 1 AuthorsF. Purrello10
Estimated H-index: 10
(University of Catania)
Background: In rat pancreatic islets, chronic exposure to high free fatty acid (FFA) levels impairs insulin secretion and β cell mass. The mechanisms underlying this defect are not completely understood. Since islets have intrinsically low anti-oxidant enzyme defense, oxidative stress might be responsible for β cell damage. Aim: In this study, we investigated if FFA could induce oxidative stress in rat pancreatic islets and if metformin might reverse adverse effects. Material and methods: We cul...
Published on May 23, 2006in Journal of Pharmacology and Experimental Therapeutics 3.62
Takanori Kudo1
Estimated H-index: 1
,
Jie Wu32
Estimated H-index: 32
+ 6 AuthorsMakoto Wakui18
Estimated H-index: 18
A sustained, high circulating level of free fatty acids (FFAs) is an important risk factor for the development of insulin resistance, islet β-cell dysfunction, and pathogenesis of type 2 diabetes. Here, we report a novel mechanism of chronic exposure of oleic acid (OA)-induced rat insulin release impairment. Following a 4-day exposure to 0.1 mM OA, there was no significant difference in basal insulin release when comparing OA-treated and untreated islets in the presence of 2.8 mM glucose, wherea...
Published on Oct 1, 2005in Clinical Diabetes
Janet H. Southerland12
Estimated H-index: 12
(UNC: University of North Carolina at Chapel Hill),
George W. Taylor Dmd DrPH38
Estimated H-index: 38
(UM: University of Michigan),
Steven Offenbacher77
Estimated H-index: 77
IN BRIEF This review focuses on the relationship between diabetes and periodontal infection and potential mechanisms involved in local and systemic disease progression. In addition, various oral complications of diabetes are discussed, along with recommendations for management, treatment, and proper referral.
Published on Sep 1, 2005in Life Sciences 3.45
Ya-liZHANG2
Estimated H-index: 2
(PKU: Peking University),
Meifang Xiao13
Estimated H-index: 13
(PKU: Peking University)
+ 1 AuthorsHuanran Tan9
Estimated H-index: 9
(PKU: Peking University)
Abstract Obesity is highly associated with type 2 diabetes where free fatty acids (FFAs) may be a trigger factor. To examine this hypothesis, in this study, we investigated the role of FFAs in the pathogenic development of type 2 diabetes. The release of insulin, the expression of preproinsulin (PPI), glucose transporter2 (GLUT2) and pancreatic duodenal homeobox-1 (PDX-1), and levels of intracellular free Ca ++ ([Ca ++ ] i ) were measured in rat pancreatic islets treated with or without high con...
Published on May 4, 2004
Lori B. Hays5
Estimated H-index: 5
The file named "hayslori.pdf" is the primary dissertation file. All other files ("*.mov") are supplemental files and may be viewed individually.
Published on Jan 1, 2004
Yan Yang (UT: University of Toledo)
Published on Oct 1, 2003in Diabetologia 7.11
G. C. Yaney1
Estimated H-index: 1
,
B. E. Corkey1
Estimated H-index: 1
Increases in glucose or fatty acids affect metabolism via changes in long-chain acyl-CoA formation and chronically elevated fatty acids increase total cellular CoA. Understanding the response of pancreatic beta cells to increased amounts of fuel and the role that altered insulin secretion plays in the development and maintenance of obesity and Type 2 diabetes is important. Data indicate that the activated form of fatty acids acts as an effector molecule in stimulus-secretion coupling. Glucose in...