High-fat diet-induced hyperglycemia and obesity in mice: Differential effects of dietary oils

Ikemoto, Shinji; Takáhashi, Mayumí; Tsunoda, Nobuyo; Maruyama, Kayo; Itakura, Hiroshige; Ezaki, Osamu

doi:10.1016/s0026-0495(96)90185-7

Cited by 254 publications

(211 citation statements)

References 52 publications

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“…Several studies report that the intake of high-fat diets containing fatty acids from fish oil high in n-3 PUFA limits the hypertrophy of fat depots compared with the intake of high-fat diets containing lard or beef tallow in rats (Parrish et al 1990(Parrish et al , 1991Belzung et al 1993;Hainault et al 1993). Similar results have been obtained with several animal models such as obese Zucker rats (Carlotti et al 1993), mice (Ikemoto et al 1996), obese ob/ob mice (Cunnane et al 1986), hamsters (Jones, 1989), and also in human subjects (Couet et al 1997). Feeding fish oil for about 1 month limits the hypertrophy of retroperitoneal and epididymal adipose tissues in rats compared with a diet containing the same amount of lard when the energy intake is similar (Parrish et al 1991;Belzung et al 1993).…”

Section: Effect Of Polyunsaturated Fatty Acids On Body Fat Accumulationsupporting

confidence: 61%

Selectivity of fatty acids on lipid metabolism and gene expression

Raclot¹,

Oudart²

1999

Proc. Nutr. Soc.

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Triacylglycerols represent the main form of storage for a wide spectrum of fatty acids. Their utilization first involves mobilization from adipose tissue through lipolysis. The release of individual fatty acids from adipose tissue is selective in vitro and in vivo in animal studies and also in human subjects. Generally, fatty acids are more readily mobilized from fat cells when they are short-chain and unsaturated. This selectivity could affect the storage of individual fatty acids in adipose tissue, and their subsequent supply to tissues. The nature of the dietary fats could affect lipid homeostasis and body fat deposition. Dietary fish oil influences adipose tissue development in a site-specific manner as a function of diet and feeding period. A diet high in n-3 polyunsaturated fatty acids (PUFA) results in a preferential partitioning of ingested energy towards oxidation at the expense of storage. Fatty acids are important mediators of gene expression in the liver. Indeed, genes encoding both glycolytic and lipogenic enzymes and key metabolic enzymes involved in fatty acid oxidation are regulated by dietary PUFA. White adipose tissue could also be a target for PUFA control of gene expression. The treatment of pre-adipose cells by fatty acids induces the expression of numerous genes that encode proteins involved in fatty acid metabolism. The mechanisms of PUFA-mediated repression of gene expression in adipocytes seem to be different, at least partly, from those described in liver. Tissue-specific and site-specific factors are possibly involved in the specific effect of PUFA on gene expression, although other mechanisms cannot be excluded.

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Section: Effect Of Polyunsaturated Fatty Acids On Body Fat Accumulationsupporting

confidence: 61%

Selectivity of fatty acids on lipid metabolism and gene expression

Raclot¹,

Oudart²

1999

Proc. Nutr. Soc.

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“…However, n-3 LC-PUFA appear to have little effect on glycaemic control in diabetic patients [4,6,7]. In rodents fed a high-fat diet, n -3 LC-PUFA efficiently prevented development of obesity [8][9][10] and of impaired glucose tolerance (IGT) [11,12].…”

Section: Introductionmentioning

confidence: 99%

n-3 Fatty acids and rosiglitazone improve insulin sensitivity through additive stimulatory effects on muscle glycogen synthesis in mice fed a high-fat diet

et al. 2009

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Aims/hypothesis Fatty acids of marine origin, i.e. docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) act as hypolipidaemics, but they do not improve glycaemic control in obese and diabetic patients. Thiazolidinediones like rosiglitazone are specific activators of peroxisome proliferator-activated receptor γ, which improve wholebody insulin sensitivity. We hypothesised that a combined treatment with a DHA and EPA concentrate (DHA/EPA) and rosiglitazone would correct, by complementary additive mechanisms, impairments of lipid and glucose homeostasis in obesity.Methods Male C57BL/6 mice were fed a corn oil-based high-fat diet. The effects of DHA/EPA (replacing 15% dietary lipids), rosiglitazone (10 mg/kg diet) or a combination of both on body weight, adiposity, metabolic markers and adiponectin in plasma, as well as on liver and muscle gene expression and metabolism were analysed. Euglycaemic-hyperinsulinaemic clamps were used to characterise the changes in insulin sensitivity. The effects of the treatments were also analysed in dietary obese mice with impaired glucose tolerance (IGT). Results DHA/EPA and rosiglitazone exerted additive effects in prevention of obesity, adipocyte hypertrophy, Diabetologia (2009) 52:941-951

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“…In particular, long-chain (LC) PUFA of the n-3 series, DHA (22: 6n-3) and EPA (20: 5n-3), which are abundant in marine fish, lower TAG while increasing HDL-cholesterol levels in plasma, prevent the development of heart disease and exert anti-inflammatory properties in human Proceedings of the Nutrition Society subjects (5)(6)(7) . Studies in rats and mice fed a high-fat or lipogenic sucrose-rich diet have shown that n-3 LC PUFA counteract the development of both obesity and insulin resistance (8)(9)(10)(11)(12)(13) . Also, in human subjects n-3 LC PUFA could reduce fat accumulation and improve glucose metabolism (14)(15)(16) .…”

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confidence: 99%

n-3 PUFA: bioavailability and modulation of adipose tissue function

et al. 2009

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Adipose tissue has a key role in the development of metabolic syndrome (MS), which includes obesity, type 2 diabetes, dyslipidaemia, hypertension and other disorders. Systemic insulin resistance represents a major factor contributing to the development of MS in obesity. The resistance is precipitated by impaired adipose tissue glucose and lipid metabolism, linked to a low-grade inflammation of adipose tissue and secretion of pro-inflammatory adipokines. Development of MS could be delayed by lifestyle modifications, while both dietary and pharmacological interventions are required for the successful therapy of MS. The n-3 long-chain (LC) PUFA, EPA and DHA, which are abundant in marine fish, act as hypolipidaemic factors, reduce cardiac events and decrease the progression of atherosclerosis. Thus, n-3 LC PUFA represent healthy constituents of diets for patients with MS. In rodents n-3 LC PUFA prevent the development of obesity and impaired glucose tolerance. The effects of n-3 LC PUFA are mediated transcriptionally by AMP-activated protein kinase and by other mechanisms. n-3 LC PUFA activate a metabolic switch toward lipid catabolism and suppression of lipogenesis, i.e. in the liver, adipose tissue and small intestine. This metabolic switch improves dyslipidaemia and reduces ectopic deposition of lipids, resulting in improved insulin signalling. Despite a relatively low accumulation of n-3 LC PUFA in adipose tissue lipids, adipose tissue is specifically linked to the beneficial effects of n-3 LC PUFA, as indicated by (1) the prevention of adipose tissue hyperplasia and hypertrophy, (2) the induction of mitochondrial biogenesis in adipocytes, (3) the induction of adiponectin and (4) the amelioration of adipose tissue inflammation by n-3 LC PUFA.

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High-fat diet-induced hyperglycemia and obesity in mice: Differential effects of dietary oils

Cited by 254 publications

References 52 publications

Selectivity of fatty acids on lipid metabolism and gene expression

Selectivity of fatty acids on lipid metabolism and gene expression

n-3 Fatty acids and rosiglitazone improve insulin sensitivity through additive stimulatory effects on muscle glycogen synthesis in mice fed a high-fat diet

n-3 PUFA: bioavailability and modulation of adipose tissue function

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