Effects of glucose-dependent insulinotropic peptide on behavior

Ding, Kai; Zhong, Qing; Xie, Dongdong; Chen, Huan Xin; Della‐Fera, Mary Anne; Bollag, Roni J.; Bollag, Wendy B.; Gujral, Ravinder; Kang, Baolin; Sridhar, Supriya; Baile, Clifton A.; Curl, Walton W.; lsales, Carlos M.

doi:10.1016/j.peptides.2006.05.011

Cited by 55 publications

(47 citation statements)

References 9 publications

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“…(5,6) We have previously reported on the development and characterization of GIP-overexpressing transgenic (Tg + ) mice. (4,7) These Tg + mice have increased bone mass consistent with our in vitro data showing stimulatory GIP effects on osteoblasts and inhibitory effects on osteoclasts. Although GIP is only one of several enteric hormones that can modulate bone mass, (8,9) our data are consistent with GIP being an important hormonal link between nutrient ingestion and bone formation.…”

Section: G Lucose-dependent Insulinotropic Peptide (Gip) Issupporting

confidence: 88%

Impact of Glucose-Dependent Insulinotropic Peptide on Age-Induced Bone Loss

Ding

Shi

Zhong

et al. 2008

Journal of Bone and Mineral Research

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Section: G Lucose-dependent Insulinotropic Peptide (Gip) Issupporting

confidence: 88%

Impact of Glucose-Dependent Insulinotropic Peptide on Age-Induced Bone Loss

Ding

Shi

Zhong

et al. 2008

Journal of Bone and Mineral Research

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“…Furthermore, overexpression of GIP in transgenic mice has actually been linked to enhanced locomotor activity [32]. Accordingly, we believe that blockade of metabolic actions of GIP consequent to increased dietary fat intake is very largely responsible for energy dissipation.…”

Section: Discussionmentioning

confidence: 95%

Chemical gastric inhibitory polypeptide receptor antagonism protects against obesity, insulin resistance, glucose intolerance and associated disturbances in mice fed high-fat and cafeteria diets

et al. 2007

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Aims/hypothesis Gastric inhibitory polypeptide (GIP) receptor antagonism with (Pro 3 )GIP improves glucose tolerance and ameliorates insulin resistance and abnormalities of islet structure/function in ob/ob mice. This study examined the ability of (Pro 3 )GIP to counter the development of obesity, insulin resistance and diabetes in mice fed high-fat and cafeteria diets. Materials and methods Young Swiss TO mice on standard chow or high-fat, cafeteria or high-carbohydrate diets received daily injections of either saline or (Pro 3 )GIP (25 nmol kg -1 day -1 ) over 16 weeks. Food intake, body weight, and circulating glucose and insulin were measured frequently. At 16 weeks, glucose tolerance, insulin sensitivity, HbA 1c , circulating hormones and plasma lipids were assessed. Adipose tissue, liver and muscle were excised and weighed, and their histology and triacylglycerol content were further examined.

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“…Further, apart from dietary fat, dietary carbohydrates are the main physiological stimulators of GIP secretion [34,35]. Therefore, diets varying in carbohydrate absorption and as such GI could have diverse effects in wild-type vs Gipr deficient states, thereby modulating insulin secretion, fat metabolism, and locomotor activity [19,20,34,35].…”

Section: Discussionmentioning

confidence: 99%

“…GIP is released following fat or carbohydrate consumption and modulates insulin secretion, as well as fat metabolism [19] and locomotor activity [20]. We have recently shown that deficiency of the GIP receptor (Gipr) also affects cumulative food intake, at least in the estrogen deficient state [21].…”

Section: Introductionmentioning

confidence: 99%

“…To test these hypotheses, we performed a [20][21][22][23][24][25][26] weeks dietary intervention study exposing young-adult (16 weeks) vs aged (44 weeks) male wild-type (C57BL/6J) and Gipr-/-mice to otherwise identical high-carbohydrate diets only differing in GI. Effects of the diets on body composition and markers of insulin sensitivity and substrate oxidation were investigated in all groups of mice.…”

Section: Introductionmentioning

confidence: 99%

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Metabolic effects of diets differing in glycaemic index depend on age and endogenous glucose-dependent insulinotrophic polypeptide in mice

et al. 2009

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Word count: abstract 243, main text 3929 3 Abstract Aims/hypothesis: High vs low glycaemic-index (GI) diets unfavourably affect body fat mass and metabolic markers in rodents. Different effects of these diets could be age-dependent, as well as mediated, in part, by carbohydrate-induced stimulation of glucose-dependent insulinotropic polypetide (GIP) signalling. Methods: Young-adult (16 weeks) and aged (44 weeks) male wild-type (C57BL/6J) and GIP-receptor knock-out (Gipr-/-) mice were exposed to otherwise identical high-carbohydrate diets only differing in GI (20-26 weeks intervention, n=8-10/group). Diet-induced changes in body fat distribution, liver fat, locomotor activity, markers of insulin sensitivity and substrate oxidation were investigated, as well as changes in the gene expression of anorexigenic and orexigenic hypothalamic factors related to food intake. Results: Body weight significantly increased in young-adult high vs low-GI fed mice (two-way ANOVA, p<0.001), regardless the Gipr genotype. The high-GI diet in young-adult mice also led to significantly increased fat mass and changes in metabolic markers that indicate reduced insulin sensitivity. Even though body fat mass also slightly increased in high vs low-GI fed aged wild-type mice (p<0.05), there were no significant changes in body weight and estimated insulin sensitivity in these animals. However, aged Gipr-/-vs wild-type mice on high-GI diet showed significantly lower cumulative net energy intake, increased locomotor activity, and improved markers of insulin sensitivity. Conclusions: The metabolic benefits of a low-GI diet appear to be more pronounced in younger animals, regardless the Gipr genotype. Inactivation of GIP signalling in aged animals on a high-GI diet, however, could be beneficial.4

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Effects of glucose-dependent insulinotropic peptide on behavior

Cited by 55 publications

References 9 publications

Impact of Glucose-Dependent Insulinotropic Peptide on Age-Induced Bone Loss

Impact of Glucose-Dependent Insulinotropic Peptide on Age-Induced Bone Loss

Chemical gastric inhibitory polypeptide receptor antagonism protects against obesity, insulin resistance, glucose intolerance and associated disturbances in mice fed high-fat and cafeteria diets

Metabolic effects of diets differing in glycaemic index depend on age and endogenous glucose-dependent insulinotrophic polypeptide in mice

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