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 inDiabetes (New York, N.Y.) Vol. 63; no. 7; pp. 2332 - 2343
Main Authors Nasteska, Daniela, Harada, Norio, Suzuki, Kazuyo, Yamane, Shunsuke, Hamasaki, Akihiro, Joo, Erina, Iwasaki, Kanako, Shibue, Kimitaka, Harada, Takanari, Inagaki, Nobuya
Format Journal Article
LanguageEnglish
Published Alexandria, VA American Diabetes Association 01.07.2014
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ISSN0012-1797
1939-327X
1939-327X
DOI10.2337/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.
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
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  surname: Nasteska
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  organization: Department of Diabetes, Endocrinology and Nutrition, Graduate School of Medicine, Kyoto University, Kyoto, Japan
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  fullname: Harada, Norio
  organization: Department of Diabetes, Endocrinology and Nutrition, Graduate School of Medicine, Kyoto University, Kyoto, Japan
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  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
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  givenname: Erina
  surname: Joo
  fullname: Joo, Erina
  organization: Department of Diabetes, Endocrinology and Nutrition, Graduate School of Medicine, Kyoto University, Kyoto, Japan
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  givenname: Kanako
  surname: Iwasaki
  fullname: Iwasaki, Kanako
  organization: Department of Diabetes, Endocrinology and Nutrition, Graduate School of Medicine, Kyoto University, Kyoto, Japan
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  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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https://www.ncbi.nlm.nih.gov/pubmed/24584548$$D View this record in MEDLINE/PubMed
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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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2014 by the American Diabetes Association.
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Issue 7
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
Language English
License CC BY 4.0
2014 by the American Diabetes Association.
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  year: 2014
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  day: 01
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PublicationPlace Alexandria, VA
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PublicationTitle Diabetes (New York, N.Y.)
PublicationTitleAlternate Diabetes
PublicationYear 2014
Publisher American Diabetes Association
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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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