Cholate inhibits high-fat diet-induced hyperglycemia and obesity with acyl-CoA synthetase mRNA decrease

Ikemoto, Shinji; Takáhashi, Mayumí; Tsunoda, Nobuyo; Maruyama, Kayo; Itakura, Hiroshige; Kawanaka, Kentaro; Tabata, Izumi; Higuchi, Mitsuru; Tange, Tsuyoshi; Yamamoto, Tokuo; Ezaki, Osamu

doi:10.1152/ajpendo.1997.273.1.e37

Cited by 45 publications

(41 citation statements)

References 30 publications

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“…Bile acids strongly affect metabolism and energy expenditure in mice (11,12,20). From studies in rats, it is known that supplementing low fat, casein-based diets with rather high doses of glycine and/or taurine affects bile acid metabolism (29,70,71).…”

Section: Discussionmentioning

confidence: 99%

“…Nutritional Regulation of Endogenous BA Metabolism Modulates High Fat Diet-induced Hyperglycemia-Oral BA treatment reduces hyperglycemia in mice (12), possibly through reduced hepatic glucose output by repression of the Pck1 gene expression (13,14). In addition, PPAR␤/␦ activation reduces hepatic glucose output and improves peripheral glucose disposal (67).…”

Section: Nutritional Regulation Of Endogenous Ba Metabolism Modulatesmentioning

confidence: 99%

“…Glucose metabolism is also regulated by bile acids, and mice treated with cholic acid are protected from diet-induced hyperglycemia (12) and have down-regulated liver expression of the gluconeogenic phosphoenolpyruvate carboxykinase (Pck1) gene (13,14). Furthermore, Fxr Ϫ/Ϫ mice are glucose-intolerant and insulin-resistant, and insulin signaling is blunted in several tissues (15)(16)(17).…”

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confidence: 99%

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Nutritional Regulation of Bile Acid Metabolism Is Associated with Improved Pathological Characteristics of the Metabolic Syndrome

Liaset¹,

Qin

Jørgensen

et al. 2011

Journal of Biological Chemistry

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Bile acids (BAs) are powerful regulators of metabolism, and mice treated orally with cholic acid are protected from dietinduced obesity, hepatic lipid accumulation, and increased plasma triacylglycerol (TAG) and glucose levels. Here, we show that plasma BA concentration in rats was elevated by exchanging the dietary protein source from casein to salmon protein hydrolysate (SPH). Importantly, the SPH-treated rats were resistant to diet-induced obesity. SPH-treated rats had reduced fed state plasma glucose and TAG levels and lower TAG in liver. The elevated plasma BA concentration was associated with induction of genes involved in energy metabolism and uncoupling, Dio2, Pgc-1␣, and Ucp1, in interscapular brown adipose tissue. Interestingly, the same transcriptional pattern was found in white adipose tissue depots of both abdominal and subcutaneous origin. Accordingly, rats fed SPH-based diet exhibited increased whole body energy expenditure and heat dissipation. In skeletal muscle, expressions of the peroxisome proliferatoractivated receptor ␤/␦ target genes (Cpt-1b, Angptl4, Adrp, and Ucp3) were induced. Pharmacological removal of BAs by inclusion of 0.5 weight % cholestyramine to the high fat SPH diet attenuated the reduction in abdominal obesity, the reduction in liver TAG, and the decrease in nonfasted plasma TAG and glucose levels. Induction of Ucp3 gene expression in muscle by SPH treatment was completely abolished by cholestyramine inclusion. Taken together, our data provide evidence that bile acid metabolism can be modulated by diet and that such modulation may prevent/ameliorate the characteristic features of the metabolic syndrome.

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Section: Discussionmentioning

confidence: 99%

Section: Nutritional Regulation Of Endogenous Ba Metabolism Modulatesmentioning

confidence: 99%

mentioning

confidence: 99%

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Nutritional Regulation of Bile Acid Metabolism Is Associated with Improved Pathological Characteristics of the Metabolic Syndrome

Liaset¹,

Qin

Jørgensen

et al. 2011

Journal of Biological Chemistry

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“…When overexpressed in hepatocytes, transcriptional regulator liver X receptor ␣, which directly senses diverse lipid metabolites as ligands (38), elevates mouse serum lipid profiles on a normal diet but improves high blood lipid profiles and protects from atherosclerosis in mice on a Western diet (39). It should also be noted that bile acids reduce high-fat diet-induced hyperglycemia and triglyceride accumulation in liver (36). FGFR4 Ϫ/Ϫ mice display increased bile acid levels (20).…”

Section: Discussionmentioning

confidence: 99%

FGFR4 Prevents Hyperlipidemia and Insulin Resistance but Underlies High-Fat Diet–Induced Fatty Liver

et al. 2007

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OBJECTIVE-Fibroblast growth factor (FGF) family signaling largely controls cellular homeostasis through short-range intercell paracrine communication. Recently FGF15/19, 21, and 23 have been implicated in endocrine control of metabolic homeostasis. The identity and location of the FGF receptor isotypes that mediate these effects are unclear. The objective was to determine the role of FGFR4, an isotype that has been proposed to mediate an ileal FGF15/19 to hepatocyte FGFR4 axis in cholesterol homeostasis, in metabolic homeostasis in vivo. RESEARCH DESIGN AND METHODS-FGFR4Ϫ/Ϫ micemice overexpressing constitutively active hepatic FGFR4 -and FGFR4 Ϫ/Ϫ with constitutively active hepatic FGFR4 restored in the liver were subjected to a normal and a chronic high-fat diet sufficient to result in obesity. Systemic and liver-specific metabolic phenotypes were then characterized. RESULTS-FGFR4-deficient mice on a normal diet exhibited features of metabolic syndrome that include increased mass of white adipose tissue, hyperlipidemia, glucose intolerance, and insulin resistance, in addition to hypercholesterolemia. Surprisingly, the FGFR4 deficiency alleviated high-fat diet-induced fatty liver in obese mice, which is also a correlate of metabolic syndrome. Restoration of FGFR4, specifically in hepatocytes of FGFR4-deficient mice, decreased plasma lipid levels and restored the high-fat diet-induced fatty liver but failed to restore glucose tolerance and sensitivity to insulin. CONCLUSIONS-FGFR4plays essential roles in systemic lipid and glucose homeostasis. FGFR4 activity in hepatocytes that normally serves to prevent systemic hyperlipidemia paradoxically underlies the fatty liver disease associated with chronic high-fat intake and obesity. Diabetes

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“…BAs are known regulators of energy homeostasis and glucose metabolism that have been reported to inhibit dietinduced obesity and prevent the development of insulin resistance (Ikemoto et al 1997, Kobayashi et al 2007, Keitel et al 2008b. Watanabe et al (2006) have shown that administration of BAs to mice increases energy expenditure in BAT, preventing obesity and insulin resistance.…”

Section: Introductionmentioning

confidence: 99%

Gender-dependent effect of Gpbar1 genetic deletion on the metabolic profiles of diet-induced obese mice

Vassileva

Hu²,

Hoos³

et al. 2010

Journal of Endocrinology

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G-protein-coupled bile acid receptor 1 (GPBAR1/TGR5/ M-Bar/GPR131) is a cell surface receptor involved in the regulation of bile acid metabolism. We have previously shown that Gpbar1-null mice are resistant to cholesterol gallstone disease when fed a lithogenic diet. Other published studies have suggested that Gpbar1 is involved in both energy homeostasis and glucose homeostasis. Here, we examine the functional role of Gpbar1 in diet-induced obese mice. We found that body weight, food intake, and fasted blood glucose levels were similar between Gpbar1-null mice and their wild-type (WT) littermates when fed a chow or high-fat diet (HFD) for 2 months. However, insulin tolerance tests revealed improved insulin sensitivity in male Gpbar1 K/K mice fed chow, but impaired insulin sensitivity when fed a HFD. In contrast, female Gpbar1 K/K mice exhibited improved insulin sensitivity when fed a HFD compared with their WT littermates. Female Gpbar1 K/K mice had significantly lower plasma cholesterol and triglyceride levels than their WT littermates on both diets. Male Gpbar1 K/K mice on HFD displayed increased hepatic steatosis when compared with Gpbar1 C/C males and Gpbar1 K/K females on HFD. These results suggest a gender-dependent regulation of Gpbar1 function in metabolic disease.

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Cholate inhibits high-fat diet-induced hyperglycemia and obesity with acyl-CoA synthetase mRNA decrease

Cited by 45 publications

References 30 publications

Nutritional Regulation of Bile Acid Metabolism Is Associated with Improved Pathological Characteristics of the Metabolic Syndrome

Nutritional Regulation of Bile Acid Metabolism Is Associated with Improved Pathological Characteristics of the Metabolic Syndrome

FGFR4 Prevents Hyperlipidemia and Insulin Resistance but Underlies High-Fat Diet–Induced Fatty Liver

Gender-dependent effect of Gpbar1 genetic deletion on the metabolic profiles of diet-induced obese mice

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