Chronic Reduction of GIP Secretion Alleviates Obesity and Insulin Resistance Under High-Fat Diet Conditions
Gastric inhibitory polypeptide (GIP) exhibits potent insulinotropic effects on β-cells and anabolic effects on bone formation and fat accumulation. We explored the impact of reduced GIP levels in vivo on glucose homeostasis, bone formation, and fat accumulation in a novel GIP-GFP knock-in (KI) mouse...
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Published in | Diabetes (New York, N.Y.) Vol. 63; no. 7; pp. 2332 - 2343 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Alexandria, VA
American Diabetes Association
01.07.2014
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Subjects | |
Online Access | Get full text |
ISSN | 0012-1797 1939-327X 1939-327X |
DOI | 10.2337/db13-1563 |
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Abstract | Gastric inhibitory polypeptide (GIP) exhibits potent insulinotropic effects on β-cells and anabolic effects on bone formation and fat accumulation. We explored the impact of reduced GIP levels in vivo on glucose homeostasis, bone formation, and fat accumulation in a novel GIP-GFP knock-in (KI) mouse. We generated GIP-GFP KI mice with a truncated prepro-GIP gene. The phenotype was assessed in heterozygous and homozygous states in mice on a control fat diet and a high-fat diet (HFD) in vivo and in vitro. Heterozygous GIP-GFP KI mice (GIP-reduced mice [GIPgfp/+]) exhibited reduced GIP secretion; in the homozygous state (GIP-lacking mice [GIPgfp/gfp]), GIP secretion was undetectable. When fed standard chow, GIPgfp/+ and GIPgfp/gfp mice showed mild glucose intolerance with decreased insulin levels; bone volume was decreased in GIPgfp/gfp mice and preserved in GIPgfp/+ mice. Under an HFD, glucose levels during an oral glucose tolerance test were similar in wild-type, GIPgfp/+, and GIPgfp/gfp mice, while insulin secretion remained lower. GIPgfp/+ and GIPgfp/gfp mice showed reduced obesity and reduced insulin resistance, accompanied by higher fat oxidation and energy expenditure. GIP-reduced mice demonstrate that partial reduction of GIP does not extensively alter glucose tolerance, but it alleviates obesity and lessens the degree of insulin resistance under HFD conditions, suggesting a potential therapeutic value. |
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AbstractList | Gastric inhibitory polypeptide (GIP) exhibits potent insulinotropic effects on β-cells and anabolic effects on bone formation and fat accumulation. We explored the impact of reduced GIP levels in vivo on glucose homeostasis, bone formation, and fat accumulation in a novel GIP-GFP knock-in (KI) mouse. We generated GIP-GFP KI mice with a truncated prepro-GIP gene. The phenotype was assessed in heterozygous and homozygous states in mice on a control fat diet and a high-fat diet (HFD) in vivo and in vitro. Heterozygous GIP-GFP KI mice (GIP-reduced mice [GIP...]) exhibited reduced GIP secretion; in the homozygous state (GIP-lacking mice [GIP...]), GIP secretion was undetectable. When fed standard chow, GIP... and GIP... mice showed mild glucose intolerance with decreased insulin levels; bone volume was decreased in GIPgfp/gfp mice and preserved in GIP... mice. Under an HFD, glucose levels during an oral glucose tolerance test were similar in wild-type, GIP..., and GIP... mice, while insulin secretion remained lower. GIP... and GIP... mice showed reduced obesity and reduced insulin resistance, accompanied by higher fat oxidation and energy expenditure. GIP-reduced mice demonstrate that partial reduction of GIP does not extensively alter glucose tolerance, but it alleviates obesity and lessens the degree of insulin resistance under HFD conditions, suggesting a potential therapeutic value. (ProQuest: ... denotes formulae/symbols omitted.) Gastric inhibitory polypeptide (GIP) exhibits potent insulinotropic effects on β-cells and anabolic effects on bone formation and fat accumulation. We explored the impact of reduced GIP levels in vivo on glucose homeostasis, bone formation, and fat accumulation in a novel GIP-GFP knock-in (KI) mouse. We generated GIP-GFP KI mice with a truncated prepro-GIP gene. The phenotype was assessed in heterozygous and homozygous states in mice on a control fat diet and a high-fat diet (HFD) in vivo and in vitro. Heterozygous GIP-GFP KI mice (GIP-reduced mice [GIPgfp/+]) exhibited reduced GIP secretion; in the homozygous state (GIP-lacking mice [GIPgfp/gfp]), GIP secretion was undetectable. When fed standard chow, GIPgfp/+ and GIPgfp/gfp mice showed mild glucose intolerance with decreased insulin levels; bone volume was decreased in GIPgfp/gfp mice and preserved in GIPgfp/+ mice. Under an HFD, glucose levels during an oral glucose tolerance test were similar in wild-type, GIPgfp/+, and GIPgfp/gfp mice, while insulin secretion remained lower. GIPgfp/+ and GIPgfp/gfp mice showed reduced obesity and reduced insulin resistance, accompanied by higher fat oxidation and energy expenditure. GIP-reduced mice demonstrate that partial reduction of GIP does not extensively alter glucose tolerance, but it alleviates obesity and lessens the degree of insulin resistance under HFD conditions, suggesting a potential therapeutic value. Gastric inhibitory polypeptide (GIP) exhibits potent insulinotropic effects on β-cells and anabolic effects on bone formation and fat accumulation. We explored the impact of reduced GIP levels in vivo on glucose homeostasis, bone formation, and fat accumulation in a novel GIP-GFP knock-in (KI) mouse. We generated GIP-GFP KI mice with a truncated prepro-GIP gene. The phenotype was assessed in heterozygous and homozygous states in mice on a control fat diet and a high-fat diet (HFD) in vivo and in vitro. Heterozygous GIP-GFP KI mice (GIP-reduced mice [GIP(gfp/+)]) exhibited reduced GIP secretion; in the homozygous state (GIP-lacking mice [GIP(gfp/gfp)]), GIP secretion was undetectable. When fed standard chow, GIP(gfp/+) and GIP(gfp/gfp) mice showed mild glucose intolerance with decreased insulin levels; bone volume was decreased in GIP(gfp/gfp) mice and preserved in GIP(gfp/+) mice. Under an HFD, glucose levels during an oral glucose tolerance test were similar in wild-type, GIP(gfp/+), and GIP(gfp/gfp) mice, while insulin secretion remained lower. GIP(gfp/+) and GIP(gfp/gfp) mice showed reduced obesity and reduced insulin resistance, accompanied by higher fat oxidation and energy expenditure. GIP-reduced mice demonstrate that partial reduction of GIP does not extensively alter glucose tolerance, but it alleviates obesity and lessens the degree of insulin resistance under HFD conditions, suggesting a potential therapeutic value.Gastric inhibitory polypeptide (GIP) exhibits potent insulinotropic effects on β-cells and anabolic effects on bone formation and fat accumulation. We explored the impact of reduced GIP levels in vivo on glucose homeostasis, bone formation, and fat accumulation in a novel GIP-GFP knock-in (KI) mouse. We generated GIP-GFP KI mice with a truncated prepro-GIP gene. The phenotype was assessed in heterozygous and homozygous states in mice on a control fat diet and a high-fat diet (HFD) in vivo and in vitro. Heterozygous GIP-GFP KI mice (GIP-reduced mice [GIP(gfp/+)]) exhibited reduced GIP secretion; in the homozygous state (GIP-lacking mice [GIP(gfp/gfp)]), GIP secretion was undetectable. When fed standard chow, GIP(gfp/+) and GIP(gfp/gfp) mice showed mild glucose intolerance with decreased insulin levels; bone volume was decreased in GIP(gfp/gfp) mice and preserved in GIP(gfp/+) mice. Under an HFD, glucose levels during an oral glucose tolerance test were similar in wild-type, GIP(gfp/+), and GIP(gfp/gfp) mice, while insulin secretion remained lower. GIP(gfp/+) and GIP(gfp/gfp) mice showed reduced obesity and reduced insulin resistance, accompanied by higher fat oxidation and energy expenditure. GIP-reduced mice demonstrate that partial reduction of GIP does not extensively alter glucose tolerance, but it alleviates obesity and lessens the degree of insulin resistance under HFD conditions, suggesting a potential therapeutic value. Gastric inhibitory polypeptide (GIP) exhibits potent insulinotropic effects on β-cells and anabolic effects on bone formation and fat accumulation. We explored the impact of reduced GIP levels in vivo on glucose homeostasis, bone formation, and fat accumulation in a novel GIP-GFP knock-in (KI) mouse. We generated GIP-GFP KI mice with a truncated prepro-GIP gene. The phenotype was assessed in heterozygous and homozygous states in mice on a control fat diet and a high-fat diet (HFD) in vivo and in vitro. Heterozygous GIP-GFP KI mice (GIP-reduced mice [GIP(gfp/+)]) exhibited reduced GIP secretion; in the homozygous state (GIP-lacking mice [GIP(gfp/gfp)]), GIP secretion was undetectable. When fed standard chow, GIP(gfp/+) and GIP(gfp/gfp) mice showed mild glucose intolerance with decreased insulin levels; bone volume was decreased in GIP(gfp/gfp) mice and preserved in GIP(gfp/+) mice. Under an HFD, glucose levels during an oral glucose tolerance test were similar in wild-type, GIP(gfp/+), and GIP(gfp/gfp) mice, while insulin secretion remained lower. GIP(gfp/+) and GIP(gfp/gfp) mice showed reduced obesity and reduced insulin resistance, accompanied by higher fat oxidation and energy expenditure. GIP-reduced mice demonstrate that partial reduction of GIP does not extensively alter glucose tolerance, but it alleviates obesity and lessens the degree of insulin resistance under HFD conditions, suggesting a potential therapeutic value. |
Author | Nasteska, Daniela Harada, Norio Shibue, Kimitaka Suzuki, Kazuyo Joo, Erina Iwasaki, Kanako Harada, Takanari Inagaki, Nobuya Yamane, Shunsuke Hamasaki, Akihiro |
Author_xml | – sequence: 1 givenname: Daniela surname: Nasteska fullname: Nasteska, Daniela organization: Department of Diabetes, Endocrinology and Nutrition, Graduate School of Medicine, Kyoto University, Kyoto, Japan – sequence: 2 givenname: Norio surname: Harada fullname: Harada, Norio organization: Department of Diabetes, Endocrinology and Nutrition, Graduate School of Medicine, Kyoto University, Kyoto, Japan – sequence: 3 givenname: Kazuyo surname: Suzuki fullname: Suzuki, Kazuyo organization: Department of Diabetes, Endocrinology and Nutrition, Graduate School of Medicine, Kyoto University, Kyoto, Japan – sequence: 4 givenname: Shunsuke surname: Yamane fullname: Yamane, Shunsuke organization: Department of Diabetes, Endocrinology and Nutrition, Graduate School of Medicine, Kyoto University, Kyoto, Japan – sequence: 5 givenname: Akihiro surname: Hamasaki fullname: Hamasaki, Akihiro organization: Department of Diabetes, Endocrinology and Nutrition, Graduate School of Medicine, Kyoto University, Kyoto, Japan – sequence: 6 givenname: Erina surname: Joo fullname: Joo, Erina organization: Department of Diabetes, Endocrinology and Nutrition, Graduate School of Medicine, Kyoto University, Kyoto, Japan – sequence: 7 givenname: Kanako surname: Iwasaki fullname: Iwasaki, Kanako organization: Department of Diabetes, Endocrinology and Nutrition, Graduate School of Medicine, Kyoto University, Kyoto, Japan – sequence: 8 givenname: Kimitaka surname: Shibue fullname: Shibue, Kimitaka organization: Department of Diabetes, Endocrinology and Nutrition, Graduate School of Medicine, Kyoto University, Kyoto, Japan – sequence: 9 givenname: Takanari surname: Harada fullname: Harada, Takanari organization: Department of Diabetes, Endocrinology and Nutrition, Graduate School of Medicine, Kyoto University, Kyoto, Japan – sequence: 10 givenname: Nobuya surname: Inagaki fullname: Inagaki, Nobuya organization: Department of Diabetes, Endocrinology and Nutrition, Graduate School of Medicine, Kyoto University, Kyoto, Japan |
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Cites_doi | 10.1152/ajpendo.00358.2007 10.1007/BF00429703 10.1111/j.2040-1124.2010.00078.x 10.1210/en.2011-2170 10.1172/JCI25483 10.1016/S0016-5085(72)80144-6 10.1042/bj1880193 10.1073/pnas.96.26.14843 10.1210/endo.133.1.8319572 10.1210/endo-128-6-3175 10.1152/ajpendo.00364.2006 10.1111/jdi.12065 10.1093/jn/125.2.183 10.1016/j.bbrc.2007.09.128 10.1016/j.bbrc.2008.08.052 10.2337/db06-S011 10.2337/db07-1124 10.1111/j.1464-5491.2008.02455.x 10.1038/nm727 10.1007/s00125-008-1202-x 10.1210/me.2005-0187 10.1210/jcem-37-5-826 10.1371/journal.pone.0022814 10.1371/journal.pone.0009590 10.1152/ajpendo.00460.2007 10.1016/j.bbrc.2005.07.164 10.1053/j.gastro.2007.09.005 10.1016/j.cmet.2012.10.019 10.1152/jn.00866.2010 10.1053/j.gastro.2007.03.054 10.2337/db09-0519 10.1172/JCI200420518 10.1111/j.2040-1124.2011.00143.x 10.1074/jbc.M500540200 10.1074/jbc.M112.423137 10.1074/jbc.M710466200 10.1152/ajpendo.90440.2008 10.1016/S0165-6147(03)00031-2 |
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Copyright | 2015 INIST-CNRS 2014 by the American Diabetes Association. Copyright American Diabetes Association Jul 2014 |
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Keywords | Endocrinopathy Obesity Secretion Diabetes mellitus Nutrition disorder Metabolic diseases Feeding Target tissue resistance Chronic Gastrointestinal hormone Diet Insulin resistance Gastric inhibitory peptide Nutritional status |
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References | Baggio (2022031223273187900_B3) 2007; 132 Parker (2022031223273187900_B21) 2009; 52 Althage (2022031223273187900_B19) 2008; 283 Kieffer (2022031223273187900_B27) 2003; 24 Yamada (2022031223273187900_B6) 2006; 55 Suzuki (2022031223273187900_B15) 2013; 288 Seino (2022031223273187900_B32) 2013; 4 Yamada (2022031223273187900_B40) 2007; 364 Harada (2022031223273187900_B31) 2011; 2 Zhong (2022031223273187900_B26) 2007; 292 Creutzfeldt (2022031223273187900_B28) 1978; 14 Naitoh (2022031223273187900_B37) 2008; 376 Miyawaki (2022031223273187900_B12) 2002; 8 Tsukiyama (2022031223273187900_B13) 2006; 20 Pacheco-Pantoja (2022031223273187900_B25) 2011 Knapper (2022031223273187900_B33) 1995; 125 Mehran (2022031223273187900_B36) 2012; 16 Preitner (2022031223273187900_B16) 2004; 113 Roberge (2022031223273187900_B24) 1993; 133 Renner (2022031223273187900_B9) 2010; 59 Song (2022031223273187900_B34) 2007; 133 Flatt (2022031223273187900_B2) 2008; 25 Pederson (2022031223273187900_B4) 1972; 62 Kim (2022031223273187900_B10) 2005; 280 Parkin (2022031223273187900_B35) 1980; 188 Fujita (2022031223273187900_B20) 2008; 295 Hansotia (2022031223273187900_B29) 2007; 117 Zhou (2022031223273187900_B38) 2005; 335 Krarup (2022031223273187900_B1) 1985; 249 McClean (2022031223273187900_B14) 2007; 293 Habib (2022031223273187900_B22) 2012; 153 Faivre (2022031223273187900_B39) 2011; 105 Widenmaier (2022031223273187900_B11) 2010; 5 Miyawaki (2022031223273187900_B7) 1999; 96 Vollmer (2022031223273187900_B18) 2008; 57 Harada (2022031223273187900_B30) 2008; 294 Dupre (2022031223273187900_B5) 1973; 37 Yamane (2022031223273187900_B17) 2012; 3 Herbach (2022031223273187900_B8) 2011; 6 Brubaker (2022031223273187900_B23) 1991; 128 |
References_xml | – volume: 294 start-page: E61 year: 2008 ident: 2022031223273187900_B30 article-title: A novel GIP receptor splice variant influences GIP sensitivity of pancreatic beta-cells in obese mice publication-title: Am J Physiol Endocrinol Metab doi: 10.1152/ajpendo.00358.2007 – volume: 14 start-page: 15 year: 1978 ident: 2022031223273187900_B28 article-title: Gastric inhibitory polypeptide (GIP) and insulin in obesity: increased response to stimulation and defective feedback control of serum levels publication-title: Diabetologia doi: 10.1007/BF00429703 – volume: 2 start-page: 193 year: 2011 ident: 2022031223273187900_B31 article-title: Plasma gastric inhibitory polypeptide and glucagon-like peptide-1 levels after glucose loading are associated with different factors in Japanese subjects publication-title: J Diabetes Invest doi: 10.1111/j.2040-1124.2010.00078.x – volume: 153 start-page: 3054 year: 2012 ident: 2022031223273187900_B22 article-title: Overlap of endocrine hormone expression in the mouse intestine revealed by transcriptional profiling and flow cytometry publication-title: Endocrinology doi: 10.1210/en.2011-2170 – volume: 117 start-page: 143 year: 2007 ident: 2022031223273187900_B29 article-title: Extrapancreatic incretin receptors modulate glucose homeostasis, body weight, and energy expenditure publication-title: J Clin Invest doi: 10.1172/JCI25483 – volume: 62 start-page: 393 year: 1972 ident: 2022031223273187900_B4 article-title: Inhibition of histamine-, pentagastrin-, and insulin-stimulated canine gastric secretion by pure “gastric inhibitory polypeptide” publication-title: Gastroenterology doi: 10.1016/S0016-5085(72)80144-6 – volume: 188 start-page: 193 year: 1980 ident: 2022031223273187900_B35 article-title: Effects of glucose and insulin on the activation of lipoprotin lipase and on protein-synthesis in rat adipose tissue publication-title: Biochem J doi: 10.1042/bj1880193 – volume: 96 start-page: 14843 year: 1999 ident: 2022031223273187900_B7 article-title: Glucose intolerance caused by a defect in the entero-insular axis: a study in gastric inhibitory polypeptide receptor knockout mice publication-title: Proc Natl Acad Sci U S A doi: 10.1073/pnas.96.26.14843 – volume: 133 start-page: 233 year: 1993 ident: 2022031223273187900_B24 article-title: Regulation of intestinal proglucagon-derived peptide secretion by glucose-dependent insulinotropic peptide in a novel enteroendocrine loop publication-title: Endocrinology doi: 10.1210/endo.133.1.8319572 – volume: 128 start-page: 3175 year: 1991 ident: 2022031223273187900_B23 article-title: Regulation of intestinal proglucagon-derived peptide secretion by intestinal regulatory peptides publication-title: Endocrinology doi: 10.1210/endo-128-6-3175 – volume: 292 start-page: E543 year: 2007 ident: 2022031223273187900_B26 article-title: Effects of glucose-dependent insulinotropic peptide on osteoclast function publication-title: Am J Physiol Endocrinol Metab doi: 10.1152/ajpendo.00364.2006 – volume: 4 start-page: 108 year: 2013 ident: 2022031223273187900_B32 article-title: Glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1: incretin actions beyond the pancreas publication-title: J Diabetes Invest doi: 10.1111/jdi.12065 – volume: 125 start-page: 183 year: 1995 ident: 2022031223273187900_B33 article-title: Investigations into the actions of glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1(7-36)amide on lipoprotein lipase activity in explants of rat adipose tissue publication-title: J Nutr doi: 10.1093/jn/125.2.183 – start-page: 12 volume-title: BMC Physiol year: 2011 ident: 2022031223273187900_B25 article-title: Receptors and effects of gut hormones in three osteoblastic cell lines – volume: 364 start-page: 175 year: 2007 ident: 2022031223273187900_B40 article-title: Genetic inactivation of GIP signaling reverses aging-associated insulin resistance through body composition changes publication-title: Biochem Biophys Res Commun doi: 10.1016/j.bbrc.2007.09.128 – volume: 376 start-page: 21 year: 2008 ident: 2022031223273187900_B37 article-title: Inhibition of GIP signaling modulates adiponectin levels under high-fat diet in mice publication-title: Biochem Biophys Res Commun doi: 10.1016/j.bbrc.2008.08.052 – volume: 249 start-page: E195 year: 1985 ident: 2022031223273187900_B1 article-title: Responses and molecular heterogeneity of IR-GIP after intraduodenal glucose and fat publication-title: Am J Physiol – volume: 55 start-page: S86 year: 2006 ident: 2022031223273187900_B6 article-title: Pancreatic and extrapancreatic effects of gastric inhibitory polypeptide publication-title: Diabetes doi: 10.2337/db06-S011 – volume: 57 start-page: 678 year: 2008 ident: 2022031223273187900_B18 article-title: Predictors of incretin concentrations in subjects with normal, impaired, and diabetic glucose tolerance publication-title: Diabetes doi: 10.2337/db07-1124 – volume: 25 start-page: 759 year: 2008 ident: 2022031223273187900_B2 article-title: Dorothy Hodgkin Lecture 2008. Gastric inhibitory polypeptide (GIP) revisited: a new therapeutic target for obesity-diabetes? publication-title: Diabet Med doi: 10.1111/j.1464-5491.2008.02455.x – volume: 8 start-page: 738 year: 2002 ident: 2022031223273187900_B12 article-title: Inhibition of gastric inhibitory polypeptide signaling prevents obesity publication-title: Nat Med doi: 10.1038/nm727 – volume: 52 start-page: 289 year: 2009 ident: 2022031223273187900_B21 article-title: Nutrient-dependent secretion of glucose-dependent insulinotropic polypeptide from primary murine K cells publication-title: Diabetologia doi: 10.1007/s00125-008-1202-x – volume: 20 start-page: 1644 year: 2006 ident: 2022031223273187900_B13 article-title: Gastric inhibitory polypeptide as an endogenous factor promoting new bone formation after food ingestion publication-title: Mol Endocrinol doi: 10.1210/me.2005-0187 – volume: 37 start-page: 826 year: 1973 ident: 2022031223273187900_B5 article-title: Stimulation of insulin secretion by gastric inhibitory polypeptide in man publication-title: J Clin Endocrinol Metab doi: 10.1210/jcem-37-5-826 – volume: 6 start-page: e22814 year: 2011 ident: 2022031223273187900_B8 article-title: Postnatal development of numbers and mean sizes of pancreatic islets and beta-cells in healthy mice and GIPR(dn) transgenic diabetic mice publication-title: PLoS One doi: 10.1371/journal.pone.0022814 – volume: 5 start-page: e9590 year: 2010 ident: 2022031223273187900_B11 article-title: A GIP receptor agonist exhibits β-cell anti-apoptotic actions in rat models of diabetes resulting in improved β-cell function and glycemic control publication-title: PLoS One doi: 10.1371/journal.pone.0009590 – volume: 293 start-page: E1746 year: 2007 ident: 2022031223273187900_B14 article-title: GIP receptor antagonism reverses obesity, insulin resistance, and associated metabolic disturbances induced in mice by prolonged consumption of high-fat diet publication-title: Am J Physiol Endocrinol Metab doi: 10.1152/ajpendo.00460.2007 – volume: 335 start-page: 937 year: 2005 ident: 2022031223273187900_B38 article-title: Gastric inhibitory polypeptide modulates adiposity and fat oxidation under diminished insulin action publication-title: Biochem Biophys Res Commun doi: 10.1016/j.bbrc.2005.07.164 – volume: 133 start-page: 1796 year: 2007 ident: 2022031223273187900_B34 article-title: Glucose-dependent insulinotropic polypeptide enhances adipocyte development and glucose uptake in part through Akt activation publication-title: Gastroenterology doi: 10.1053/j.gastro.2007.09.005 – volume: 16 start-page: 723 year: 2012 ident: 2022031223273187900_B36 article-title: Hyperinsulinemia drives diet-induced obesity independently of brain insulin production publication-title: Cell Metab doi: 10.1016/j.cmet.2012.10.019 – volume: 105 start-page: 1574 year: 2011 ident: 2022031223273187900_B39 article-title: Glucose-dependent insulinotropic polypeptide receptor knockout mice are impaired in learning, synaptic plasticity, and neurogenesis publication-title: J Neurophysiol doi: 10.1152/jn.00866.2010 – volume: 132 start-page: 2131 year: 2007 ident: 2022031223273187900_B3 article-title: Biology of incretins: GLP-1 and GIP publication-title: Gastroenterology doi: 10.1053/j.gastro.2007.03.054 – volume: 59 start-page: 1228 year: 2010 ident: 2022031223273187900_B9 article-title: Glucose intolerance and reduced proliferation of pancreatic β-cells in transgenic pigs with impaired glucose-dependent insulinotropic polypeptide function publication-title: Diabetes doi: 10.2337/db09-0519 – volume: 113 start-page: 635 year: 2004 ident: 2022031223273187900_B16 article-title: Gluco-incretins control insulin secretion at multiple levels as revealed in mice lacking GLP-1 and GIP receptors publication-title: J Clin Invest doi: 10.1172/JCI200420518 – volume: 3 start-page: 80 year: 2012 ident: 2022031223273187900_B17 article-title: Effects of glucose and meal ingestion on incretin secretion in Japanese subjects with normal glucose tolerance publication-title: J Diabetes Invest doi: 10.1111/j.2040-1124.2011.00143.x – volume: 280 start-page: 22297 year: 2005 ident: 2022031223273187900_B10 article-title: Glucose-dependent insulinotropic polypeptide (GIP) stimulation of pancreatic β-cell survival is dependent upon phosphatidylinositol 3-kinase (PI3K)/protein kinase B (PKB) signaling, inactivation of the forkhead transcription factor Foxo1, and down-regulation of bax expression publication-title: J Biol Chem doi: 10.1074/jbc.M500540200 – volume: 288 start-page: 1929 year: 2013 ident: 2022031223273187900_B15 article-title: Transcriptional regulatory factor X6 (Rfx6) increases gastric inhibitory polypeptide (GIP) expression in enteroendocrine K-cells and is involved in GIP hypersecretion in high fat diet-induced obesity publication-title: J Biol Chem doi: 10.1074/jbc.M112.423137 – volume: 283 start-page: 18365 year: 2008 ident: 2022031223273187900_B19 article-title: Targeted ablation of glucose-dependent insulinotropic polypeptide-producing cells in transgenic mice reduces obesity and insulin resistance induced by a high fat diet publication-title: J Biol Chem doi: 10.1074/jbc.M710466200 – volume: 295 start-page: E648 year: 2008 ident: 2022031223273187900_B20 article-title: Pax6 and Pdx1 are required for production of glucose-dependent insulinotropic polypeptide in proglucagon-expressing L cells publication-title: Am J Physiol Endocrinol Metab doi: 10.1152/ajpendo.90440.2008 – volume: 24 start-page: 110 year: 2003 ident: 2022031223273187900_B27 article-title: GIP or not GIP? That is the question publication-title: Trends Pharmacol Sci doi: 10.1016/S0165-6147(03)00031-2 |
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Snippet | Gastric inhibitory polypeptide (GIP) exhibits potent insulinotropic effects on β-cells and anabolic effects on bone formation and fat accumulation. We explored... |
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SubjectTerms | Animals Biological and medical sciences Body Weight - genetics Diabetes. Impaired glucose tolerance Diet, High-Fat Down-Regulation - genetics Endocrine pancreas. Apud cells (diseases) Endocrinopathies Etiopathogenesis. Screening. Investigations. Target tissue resistance Gastric Inhibitory Polypeptide - genetics Gastric Inhibitory Polypeptide - secretion Gene Knock-In Techniques Genotype & phenotype Glucose Glucose - metabolism Homeostasis Insulin resistance Insulin Resistance - genetics Insulin-Secreting Cells - metabolism Male Medical sciences Metabolic diseases Mice Mice, Transgenic Obesity Obesity - metabolism Obesity - therapy Polypeptides Receptors, Gastrointestinal Hormone - genetics Receptors, Gastrointestinal Hormone - metabolism Rodents |
Title | Chronic Reduction of GIP Secretion Alleviates Obesity and Insulin Resistance Under High-Fat Diet Conditions |
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