Abstract
A calorie-dense diet is a well-established risk factor for obesity and metabolic syndrome (MetS), whereas the role of the intestinal microbiota (IMB) in the development of diet-induced obesity (DIO) is not completely understood. To test the hypothesis that Swiss Webster (Tac:SW) mice can develop characteristics of DIO and MetS in the absence of the IMB, we fed conventional (CV) and germ-free (GF) male Tac:SW mice either a low-fat diet (LFD; 10% fat derived calories) or a high-fat diet (HFD; 60% fat derived calories) for 10 weeks. The HFD increased feed conversion and body weight in GF mice independent of the increase associated with the microbiota in CV mice. In contrast to CV mice, GF mice did not decrease feed intake on the HFD and possessed heavier fat pads. The HFD caused hyperglycemia, hyperinsulinemia, and impaired glucose absorption in GF mice independent of the increase associated with the microbiota in CV mice. A HFD also elevated plasma LDL-cholesterol and increased hepatic triacylglycerol, free fatty acids, and ceramides in all mice, whereas hypertriglyceridemia and increased hepatic medium and long-chain acylcarnitines were only observed in CV mice. Therefore, GF male Tac:SW mice developed several detrimental effects of obesity and MetS from a high-fat, calorie dense diet.
Highlights
Diet-induced obesity (DIO) impairs glucose and lipid homeostasis, increases chronic systemic inflammation, causes hypertension, and is a primary risk factor for hepatic steatosis, type II diabetes mellitus (T2DM), and cardiovascular disease (CVD) [1,2,3,4,5]
Bäckhed and colleagues recently developed a simplified human intestinal microbiota (IMB) model using GF Swiss Webster mice that holds promise in the study of diet–host–microbiota interactions in relation to obesity and metabolic syndrome (MetS) [40]. To study these interactions in relation to diet-induced obesity (DIO), it is necessary to determine the role that the IMB play in the development of obesity and MetS in Swiss Webster mice
The IMB is not required for DIO in male Taconic Swiss Webster (Tac):SW mice, and the IMB allow CV male Tac:SW mice to gain weight even on the low-fat diet (LFD)
Summary
Diet-induced obesity (DIO) impairs glucose and lipid homeostasis, increases chronic systemic inflammation, causes hypertension, and is a primary risk factor for hepatic steatosis, type II diabetes mellitus (T2DM), and cardiovascular disease (CVD) [1,2,3,4,5]. Calorie-dense diets such as the high-fat and high-sucrose Western diet are a major cause of DIO in humans, and similar diets induce obesity in mouse models [9,10,11,12]. These diets are rich in simple digestible sugars, saturated lipids, or both, and possess a high fractional feed conversion. Abdominal obesity, insulin resistance, and other indicators of MetS develop with DIO [14,15,16]
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