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

Isken, Frank; Weickert, Martin O.; Tschöp, Matthias H.; Nogueiras, Rubén; Möhlig, Matthias; Abdelrahman, Ammar A.; Schimrigk, К.; Thorens, Bernard; Pfeiffer, Andreas F. H.

doi:10.1007/s00125-009-1466-9

Cited by 34 publications

(41 citation statements)

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“…We clearly see an increased cumulative food intake in KO C-C-H compared with WT C-C-H, which matches the observation that Gipr 2/2 mice use fat for energy metabolism rather than storing it in adipose tissue (5). This phenomenon was reversed when Gipr 2/2 mice were placed on an HFD during IU/L, indicating that GIP physiologically prevents increased energy expenditure in response to increased energy intake as shown earlier (7).…”

Section: Discussionsupporting

confidence: 60%

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High-Fat Diet During Mouse Pregnancy and Lactation Targets GIP-Regulated Metabolic Pathways in Adult Male Offspring

et al. 2015

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Maternal obesity is a worldwide problem associated with increased risk of metabolic diseases in the offspring. Genetic deletion of the gastric inhibitory polypeptide (GIP) receptor (GIPR) prevents high-fat diet (HFD)-induced obesity in mice due to specific changes in energy and fat cell metabolism. We investigated whether GIP-associated pathways may be targeted by fetal programming and mimicked the situation by exposing pregnant mice to control or HFD during pregnancy (intrauterine [IU]) and lactation (L). Male wild-type (WT) and Gipr 2/2 offspring received control chow until 25 weeks of age followed by 20 weeks of HFD. Gipr 2/2 offspring of mice exposed to HFD during IU/L became insulin resistant and obese and exhibited increased adipose tissue inflammation and decreased peripheral tissue substrate utilization after being reintroduced to HFD, similar to WT mice on regular chow during IU/L. They showed decreased hypothalamic insulin sensitivity compared with Gipr 2/2 mice on control diet during IU/L.DNA methylation analysis revealed increased methylation of CpG dinucleotides and differential transcription factor binding of promoter regions of genes involved in lipid oxidation in the muscle of Gipr 2/2 offspring on HFD during IU/L, which were inversely correlated with gene expression levels. Our data identify GIP-regulated metabolic pathways that are targeted by fetal programming.Gastric inhibitory polypeptide (GIP) is released from the duodenum after nutrient intake and regulates postprandial insulin secretion (1). GIP is known for its anabolic effects in adipocytes (2) and has been shown to stimulate the activity of lipoprotein lipase in adipose tissue in vitro (3) (4). Genetic ablation of the GIP receptor (GIPR) protects from high-fat diet (HFD)-induced obesity and insulin resistance in mice (5). GIPR knockout (Gipr) mice use fat as energy substrate rather than storing it in adipocytes. Moreover, central appetite-regulating pathways are downregulated in ovariectomized female Gipr 2/2 mice (6), and energy expenditure is increased in Gipr 2/2 mice exposed to a high-glycemic index diet (7) or an HFD (8).Since Gipr 2/2 mice are protected from obesity when exposed to a postweaning HFD, we hypothesized that this phenotype may be lost when these mice were exposed to the same HFD during pregnancy (intrauterine [IU]) and lactation (L). The IU milieu has a persisting influence on the development of adult diseases (9,10). Maternal caloric malnutrition as well as overnutrition during IU and L can induce metabolic disturbances later in life in offspring (11,12). Animal studies have shown that mice exposed to a maternal HFD during IU/L and weaned onto a standard chow developed adiposity, insulin resistance, and hepatosteatosis later in life (13,14). Not only the diet during IU/L but also the postweaning diet is important for the manifestation of metabolic diseases. Studies investigating the interaction of an HFD during IU/L and postweaning usually apply the HFD continuously from premating throughout the end of the study in ...

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Section: Discussionsupporting

confidence: 60%

“…Moreover, central appetite-regulating pathways are downregulated in ovariectomized female Gipr 2/2 mice (6), and energy expenditure is increased in Gipr 2/2 mice exposed to a high-glycemic index diet (7) or an HFD (8).…”

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High-Fat Diet During Mouse Pregnancy and Lactation Targets GIP-Regulated Metabolic Pathways in Adult Male Offspring

et al. 2015

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“…Before the main experiments, postprandial glucose and insulin responses to the here used experimental high (100% amylopectin, 0% amylose) vs. low (30% amylopectin, 70% amylose) GI diets were tested in a trained meal test with a separate group of male C57BL/6J mice (n ϭ 16), as detailed previously (11). Both diets contained 65% carbohydrate, 23% protein, and 12% fat.…”

Section: Animalsmentioning

confidence: 99%

“…Glucose tolerance tests (GTT) were performed in the long-term study after 15 wk of dietary intervention in overnight fasted mice, as detailed previously (11). Plasma was collected before and 10, 30, and 60 min after glucose challenge (2 g/kg body wt) and immediately stored at Ϫ80°C for measurement of glucose and insulin.…”

Section: Animalsmentioning

confidence: 99%

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Impairment of fat oxidation under high- vs. low-glycemic index diet occurs before the development of an obese phenotype

Isken

Klaus²,

Petzke

et al. 2010

American Journal of Physiology-Endocrinology and Metabolism

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Exposure to high vs. low glycemic index (GI) diets increases fat mass and insulin resistance in obesity-prone C57BL/6J mice. However, the longer-term effects and potentially involved mechanisms are largely unknown. We exposed four groups of male C57BL/6J mice (n ϭ 10 per group) to long-term (20 wk) or short-term (6 wk) isoenergetic and macronutrient matched diets only differing in starch type and as such GI. Body composition, liver fat, molecular factors of lipid metabolism, and markers of insulin sensitivity and metabolic flexibility were investigated in all four groups of mice. Mice fed the high GI diet showed a rapid-onset (from week 5) marked increase in body fat mass and liver fat, a gene expression profile in liver consistent with elevated lipogenesis, and, after long-term exposure, significantly reduced glucose clearance following a glucose load. The long-term high-GI diet also led to a delayed switch to both carbohydrate and fat oxidation in the postprandial state, indicating reduced metabolic flexibility. In contrast, no difference in carbohydrate oxidation was observed after short-term high-vs. low-GI exposure. However, fatty acid oxidation was significantly blunted as early as 3 wk after beginning of the high-GI intervention, at a time where most measured phenotypic markers including body fat mass were comparable between groups. Thus long-term high-GI feeding resulted in an obese, insulin-resistant, and metabolically inflexible phenotype in obesity-prone C57BL/6J mice. Early onset and significantly impaired fatty acid oxidation preceded these changes, thereby indicating a potentially causal involvement. glycemic index; fat metabolism; body fat; insulin resistance; liver fat; metabolic flexibility; insulin resistance EXPOSURE TO HIGH VS. LOW glycemic index (GI) diets unfavorably affects fat mass and markers of insulin resistance in rodent models (1, 12, 15-17, 21, 23). Metabolic flexibility that can be defined as the capacity to adapt fuel oxidation to fuel availability (3, 7, 13) could also be changed by a high-GI diet, although no consensus exists as to whether diets varying in GI directly affect substrate oxidation or energy expenditure (4, 21). Alternatively, changes in substrate oxidation might be mainly a consequence of high-vs. low-GI diet-induced differences, e.g., in body weight, body fat distribution, or insulin resistance. Therefore, elucidating whether changes in substrate oxidation follow or precede an obese phenotype in high-GI-fed animals could be helpful for the understanding of potentially involved mechanisms.Most of the previous studies investigating effects of highvs. low-GI diets on metabolic markers were relatively short term (1,12,15,16,23), lasting between 3 and up to 13 wk. We are aware of only two previous longer-term studies, both of which reported unfavorable effects of high-vs. low-GI diets on body fat distribution and metabolic markers in rodents (17, 21). However, the first study (18 wk) investigated partial pancreatectomized male Sprague-Dawley rats, which is an animal mo...

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Current literature in diabetes

2010

Diabetes Metabolism Res

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In order to keep subscribers up‐to‐date with the latest developments in their field, John Wiley & Sons are providing a current awareness service in each issue of the journal. The bibliography contains newly published material in the field of diabetes/metabolism. Each bibliography is divided into 26 sections: 1 Reviews; 2 General; 3 Genetics; 4 Epidemiology; 5 Immunology; 6 Obesity; 7 Prediction and Prevention; 8 Intervention: a) General; b) Care; c) Drug Therapy; d)Economics; e) Gene therapy; f) Nursing; g) Nutrition; h) Surgery; i) Transplantation; 9 Pathology and Complications: a) General; b) Cardiovascular; c) Eye disease; d) Gestational and fetal; e) Neurological; f) Podiatrical; g) Renal; 10 Endocrinology & Metabolism; 11 Experimental Studies; 12 Diagnosis and Techniques. Within each section, articles are listed in alphabetical order with respect to author

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

Cited by 34 publications

References 42 publications

High-Fat Diet During Mouse Pregnancy and Lactation Targets GIP-Regulated Metabolic Pathways in Adult Male Offspring

High-Fat Diet During Mouse Pregnancy and Lactation Targets GIP-Regulated Metabolic Pathways in Adult Male Offspring

Impairment of fat oxidation under high- vs. low-glycemic index diet occurs before the development of an obese phenotype

Current literature in diabetes

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