Metabolic control of -cell function

Abstract Glucose-induced insulin secretion is pulsatile. Glucose metabolism generates oscillations in the ATP/ADP ratio which lead to opening and closing of ATP-sensitive K + -channels producing subsequent oscillations in membrane potential, cytoplasmic calcium and insulin release. Metabolic signals derived from glucose can also stimulate insulin release independent of their effects on ATP-sensitive K + -channels. The ATP/ADP ratio may mediate both ATP-sensitive K + -channel-dependent and -independent pathways of secretion. Glucose metabolism also results in an increase in long-chain acyl-CoA, which is proposed to act as an effector molecule in the β -cell. Long-chain acyl-CoA has a variety of effects in the β -cell that may effect insulin secretion including opening ATP-sensitive K + -channels, activating endoplasmic reticulum Ca 2+ -ATPases and stimulating classical protein kinase C activity. In addition to stimulating insulin release, nutrients also effect gene expression, protein synthesis and β -cell proliferation. Gene expression is effected by nutrient induction of a variety of immediate early response genes. Glucose stimulates proinsulin biosynthesis both at the translational and transcriptional level. β -cell proliferation, as a result of insulin-like growth factor and growth hormone mitogenic pathways, is also glucose dependent. Thus, many β -cell functions in addition to secretion are controlled by nutrient metabolism.

[1]  B. Corkey,et al.  Long-Chain Acyl CoA Regulation of Protein Kinase C and Fatty Acid Potentiation of Glucose-Stimulated Insulin Secretion in Clonalβ -Cells. , 2000, Endocrinology.

[2]  M. Prentki,et al.  Acute Stimulation with Long Chain Acyl-CoA Enhances Exocytosis in Insulin-secreting Cells (HIT T-15 and NMRI β-Cells)* , 2000, The Journal of Biological Chemistry.

[3]  M. White,et al.  Stimulation of pancreatic beta-cell proliferation by growth hormone is glucose-dependent: signal transduction via janus kinase 2 (JAK2)/signal transducer and activator of transcription 5 (STAT5) with no crosstalk to insulin receptor substrate-mediated mitogenic signalling. , 1999, The Biochemical journal.

[4]  R. Robertson,et al.  In vivo prevention of hyperglycemia also prevents glucotoxic effects on PDX-1 and insulin gene expression. , 1999, Diabetes.

[5]  R Nano,et al.  Mechanisms of coordination of Ca2+ signals in pancreatic islet cells. , 1999, Diabetes.

[6]  M. Prentki,et al.  Palmitate and oleate induce the immediate-early response genes c-fos and nur-77 in the pancreatic beta-cell line INS-1. , 1999, Diabetes.

[7]  S. Bonner-Weir,et al.  Chronic Hyperglycemia Triggers Loss of Pancreatic β Cell Differentiation in an Animal Model of Diabetes* , 1999, The Journal of Biological Chemistry.

[8]  B. Soria,et al.  Intracellular diadenosine polyphosphates: a novel second messenger in stimulus‐secretion coupling , 1998, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[9]  J. Henquin,et al.  The K+-ATP channel-independent pathway of regulation of insulin secretion by glucose: in search of the underlying mechanism. , 1998, Diabetes.

[10]  M. Prentki,et al.  Glucose and glucoincretin peptides synergize to induce c‐fos, c‐jun, junB, zif‐268, and nur‐77 gene expression in pancreatic β(INS‐1) cells , 1998, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[11]  M. Köhler,et al.  Short-term regulation of insulin gene transcription by glucose. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[12]  Å. Sjöholm.  Aspects of novel sites of regulation of the insulin stimulus-secretion coupling in normal and diabetic pancreatic islets , 1998, Endocrine.

[13]  P. Gilon,et al.  Interplay between cytoplasmic Ca2+ and the ATP/ADP ratio: a feedback control mechanism in mouse pancreatic islets. , 1998, The Biochemical journal.

[14]  M. White,et al.  Insulin-like growth factor I (IGF-I)-stimulated pancreatic beta-cell growth is glucose-dependent. Synergistic activation of insulin receptor substrate-mediated signal transduction pathways by glucose and IGF-I in INS-1 cells. , 1998, The Journal of biological chemistry.

[15]  P. Hanson,et al.  Membrane fusion: SNAREs line up in new environment , 1998, Nature.

[16]  B. Wicksteed,et al.  A distinct difference in the metabolic stimulus-response coupling pathways for regulating proinsulin biosynthesis and insulin secretion that lies at the level of a requirement for fatty acyl moieties. , 1998, The Biochemical journal.

[17]  J. Keizer,et al.  Model of beta-cell mitochondrial calcium handling and electrical activity. II. Mitochondrial variables. , 1998, The American journal of physiology.

[18]  M. Komatsu,et al.  Palmitate and myristate selectively mimic the effect of glucose in augmenting insulin release in the absence of extracellular Ca2+. , 1998, Diabetes.

[19]  J. McGarry,et al.  Chronic exposure to free fatty acid reduces pancreatic beta cell insulin content by increasing basal insulin secretion that is not compensated for by a corresponding increase in proinsulin biosynthesis translation. , 1998, The Journal of clinical investigation.

[20]  G. Shulman,et al.  Disruption of IRS-2 causes type 2 diabetes in mice , 1998, Nature.

[21]  G. Waeber,et al.  Fatty Acids Decrease IDX-1 Expression in Rat Pancreatic Islets and Reduce GLUT2, Glucokinase, Insulin, and Somatostatin Levels* , 1997, The Journal of Biological Chemistry.

[22]  K. Tornheim.  Are Metabolic Oscillations Responsible for Normal Oscillatory Insulin Secretion? , 1997, Diabetes.

[23]  C. Xiao,et al.  Tight links between adenine and guanine nucleotide pools in mouse pancreatic islets: a study with mycophenolic acid. , 1997, The Biochemical journal.

[24]  M. Prentki,et al.  Long-Chain Fatty Acids Inhibit Acetyl-CoA Carboxylase Gene Expression in the Pancreatic β-Cell Line INS-1 , 1997, Diabetes.

[25]  R. Scheller,et al.  Hrs-2 is an ATPase implicated in calcium-regulated secretion , 1997, Nature.

[26]  M. Prentki,et al.  Induction by Glucose of Genes Coding for Glycolytic Enzymes in a Pancreatic β-Cell Line (INS-1)* , 1997, The Journal of Biological Chemistry.

[27]  M. Prentki,et al.  Fatty Acids Rapidly Induce the Carnitine Palmitoyltransferase I Gene in the Pancreatic β-Cell Line INS-1* , 1997, The Journal of Biological Chemistry.

[28]  D. Pipeleers,et al.  Glucose promotes survival of rat pancreatic beta cells by activating synthesis of proteins which suppress a constitutive apoptotic program. , 1996, The Journal of clinical investigation.

[29]  M. Prentki,et al.  Regulation of pancreatic beta-cell mitochondrial metabolism: influence of Ca2+, substrate and ADP. , 1996, The Biochemical journal.

[30]  S. Chheda,et al.  Reversible Ca2+-dependent Translocation of Protein Kinase C and Glucose-induced Insulin Release* , 1996, The Journal of Biological Chemistry.

[31]  A. Omori,et al.  Phosphorylation of 25-kDa Synaptosome-associated Protein , 1996, The Journal of Biological Chemistry.

[32]  B. Fredholm,et al.  Oscillations in KATP channel activity promote oscillations in cytoplasmic free Ca2+ concentration in the pancreatic beta cell. , 1996, Proceedings of the National Academy of Sciences of the United States of America.

[33]  O. Larsson,et al.  Activation of the ATP-sensitive K Channel by Long Chain Acyl-CoA , 1996, The Journal of Biological Chemistry.

[34]  J. Deeney,et al.  Temporal sequence of metabolic and ionic events in glucose-stimulated clonal pancreatic beta-cells (HIT). , 1996, The Biochemical journal.

[35]  J. Sturis,et al.  Seminars in Medicine of the Beth Israel Hospital, Boston. Non-insulin-dependent diabetes mellitus - a genetically programmed failure of the beta cell to compensate for insulin resistance. , 1996, The New England journal of medicine.

[36]  Å. Sjöholm.  Diabetes mellitus and impaired pancreatic β‐cell proliferation , 1996 .

[37]  M. Prentki,et al.  Are the β-Cell Signaling Molecules Malonyl-CoA and Cystolic Long-Chain Acyl-CoA Implicated in Multiple Tissue Defects of Obesity and NIDDM? , 1996, Diabetes.

[38]  M. Prentki,et al.  Evidence for an Anaplerotic/Malonyl-CoA Pathway in Pancreatic β-Cell Nutrient Signaling , 1996, Diabetes.

[39]  T. Schermerhorn,et al.  Glucose stimulation of insulin release in the absence of extracellular Ca2+ and in the absence of any increase in intracellular Ca2+ in rat pancreatic islets. , 1995, Proceedings of the National Academy of Sciences of the United States of America.

[40]  P. Hanson,et al.  The N-Ethylmaleimide-sensitive Fusion Protein and α-SNAP Induce a Conformational Change in Syntaxin (*) , 1995, The Journal of Biological Chemistry.

[41]  K. Williams,et al.  Rab3A effector domain peptides induce insulin exocytosis via a specific interaction with a cytosolic protein doublet. , 1994, The Journal of biological chemistry.

[42]  C. Wollheim,et al.  Dynamic pacing of cell metabolism by intracellular Ca2+ transients. , 1994, The Journal of biological chemistry.

[43]  P. Bergsten,et al.  Synchronous oscillations of cytoplasmic Ca2+ and insulin release in glucose-stimulated pancreatic islets. , 1994, The Journal of biological chemistry.

[44]  P. Berggren,et al.  Ca2+ and pancreatic B-cell function. , 1994, Biochemical Society transactions.

[45]  T. Pozzan,et al.  Stimulated Ca2+ influx raises mitochondrial free Ca2+ to supramicromolar levels in a pancreatic beta-cell line. Possible role in glucose and agonist-induced insulin secretion. , 1993, The Journal of biological chemistry.

[46]  P. Gilon,et al.  Oscillations of secretion driven by oscillations of cytoplasmic Ca2+ as evidences in single pancreatic islets. , 1993, The Journal of biological chemistry.

[47]  M. Prentki,et al.  Glucose regulates acetyl-CoA carboxylase gene expression in a pancreatic beta-cell line (INS-1). , 1993, The Journal of biological chemistry.

[48]  M. Prentki,et al.  Acyl-CoA esters modulate intracellular Ca2+ handling by permeabilized clonal pancreatic beta-cells. , 1992, The Journal of biological chemistry.

[49]  M. Erecińska,et al.  Energy metabolism in islets of Langerhans. , 1992, Biochimica et biophysica acta.

[50]  P. Gilon,et al.  Evidence that glucose can control insulin release independently from its action on ATP-sensitive K+ channels in mouse B cells. , 1992, The Journal of clinical investigation.

[51]  M. Prentki,et al.  Malonyl-CoA and long chain acyl-CoA esters as metabolic coupling factors in nutrient-induced insulin secretion. , 1992, The Journal of biological chemistry.

[52]  R. Hansford.  Dehydrogenase activation by Ca2+ in cells and tissues , 1991, Journal of bioenergetics and biomembranes.

[53]  B. Corkey,et al.  Protein kinase C isotypes and signaling in neutrophils. Differential substrate specificities of a translocatable calcium- and phospholipid-dependent beta-protein kinase C and a phospholipid-dependent protein kinase which is inhibited by long chain fatty acyl coenzyme A. , 1991, The Journal of biological chemistry.

[54]  F. Matschinsky,et al.  Content of CoA-Esters in Perifused Rat Islets Stimulated by Glucose and Other Fuels , 1991, Diabetes.

[55]  J. Leahy.  Natural History of β-Cell Dysfunction in NIDDM , 1990, Diabetes Care.

[56]  B. Corkey,et al.  Glucose-induced activation of pyruvate dehydrogenase in isolated rat pancreatic islets. , 1990, The Biochemical journal.

[57]  B. Wolf,et al.  Diacylglycerol synthesis de novo from glucose by pancreatic islets isolated from rats and humans. , 1990, The Journal of clinical investigation.

[58]  E. Ipp,et al.  Pulsatile Insulin Secretion in Isolated Rat Islets , 1990, Diabetes.

[59]  J. Leahy,et al.  Compensatory Growth of Pancreatic β-Cells in Adult Rats After Short-Term Glucose Infusion , 1989, Diabetes.

[60]  M. Berridge,et al.  Cytosolic calcium oscillators , 1988, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[61]  Y. Nishizuka,et al.  The molecular heterogeneity of protein kinase C and its implications for cellular regulation , 1988, Nature.

[62]  K. Polonsky,et al.  Abnormal patterns of insulin secretion in non-insulin-dependent diabetes mellitus. , 1988, The New England journal of medicine.

[63]  P. Halban,et al.  Newly synthesized proinsulin/insulin and stored insulin are released from pancreatic B cells predominantly via a regulated, rather than a constitutive, pathway , 1987, The Journal of cell biology.

[64]  H. Orskov,et al.  Glucose uptake and pulsatile insulin infusion: euglycaemic clamp and [3-3H]glucose studies in healthy subjects. , 1986, Acta endocrinologica.

[65]  H. Najafi,et al.  Identification of Glucokinase as an Alloxan-Sensitive Glucose Sensor of the Pancreatic β-Cell , 1986, Diabetes.

[66]  L. Rosário,et al.  Pulsatile insulin release and electrical activity from single ob/ob mouse islets of Langerhans. , 1986, Advances in experimental medicine and biology.

[67]  F. Matschinsky,et al.  Pancreatic islet glucose metabolism and regulation of insulin secretion. , 1986, Diabetes/metabolism reviews.

[68]  G. Reaven,et al.  Ambient plasma free fatty acid concentrations in noninsulin-dependent diabetes mellitus: evidence for insulin resistance. , 1985, The Journal of clinical endocrinology and metabolism.

[69]  F. Matschinsky,et al.  New perspectives on pancreatic islet glucokinase. , 1984, The American journal of physiology.

[70]  R. Turner,et al.  Pulsatile Insulin Has Greater Hypoglycemic Effect Than Continuous Delivery , 1983, Diabetes.

[71]  W. Malaisse,et al.  The stimulus-secretion coupling of glucose-induced insulin release: fuel metabolism in islets deprived of exogenous nutrient. , 1983, Archives of biochemistry and biophysics.

[72]  MacDonald Mj.  Calcium activation of pancreatic islet mitochondrial glycerol phosphate dehydrogenase. , 1982 .

[73]  M. J. MacDonald,et al.  Evidence for the malate aspartate shuttle in pancreatic islets. , 1982, Archives of biochemistry and biophysics.

[74]  M. Yatvin,et al.  Fatty acyl coenzyme A-sensitive adenine nucleotide transport in a reconstituted liposome system. , 1981, The Journal of biological chemistry.

[75]  G. Weir,et al.  Sustained oscillations of insulin, glucagon, and somatostatin from the isolated canine pancreas during exposure to a constant glucose concentration. , 1980, The Journal of clinical investigation.

[76]  H. Okamoto,et al.  Translational control of proinsulin synthesis by glucose , 1980, Nature.

[77]  J. McGarry,et al.  In support of the roles of malonyl-CoA and carnitine acyltransferase I in the regulation of hepatic fatty acid oxidation and ketogenesis. , 1979, The Journal of biological chemistry.

[78]  W. Malaisse,et al.  Insulin release: the fuel hypothesis. , 1979, Metabolism: clinical and experimental.

[79]  R. Bohnensack,et al.  Control of oxidative phosphorylation by the extra-mitochondrial ATP/ADP ratio. , 1976, Biochimica et biophysica acta.