Abstract
Dietary fatty acids play important roles in the regulation of fat accumulation or metabolic phenotype of adipocytes, either as brown or beige fat. However, a systematic comparison of effects of diets with different composition of 18-C fatty acids on browning/beiging phenotype has not been done. In this study, we compared the effects of different dietary fats, rich in specific 18-carbon fatty acids, on thermogenesis and lipid metabolism. Male C57BL/6 mice were fed a control diet containing 5.6% kcal fat from lard and 4.4% kcal fat from soybean oil (CON) or high-fat diets (HFD) containing 25% kcal from lard and 20% kcal fat from shea butter (stearic acid-rich fat; SHB), olive oil (oleic acid-rich oil; OO), safflower oil (linoleic acid-rich oil; SFO), or soybean oil (mixed oleic, linoleic, and α-linolenic acids; SBO) ad libitum for 12 weeks, with or without a terminal 4-h norepinephrine (NE) treatment. When compared to SHB, feeding OO, SFO, and SBO resulted in lower body weight gain. The OO fed group had the highest thermogenesis level, which resulted in lower body fat accumulation and improved glucose and lipid metabolism. Feeding SFO downregulated expression of lipid oxidation-related genes and upregulated expression of lipogenic genes, perhaps due to its high n-6:n-3 ratio. In general, HFD-feeding downregulated Ucp1 expression in both subcutaneous and epididymal white adipose tissue, and suppressed NE-induced Pgc1a expression in brown adipose tissue. These results suggest that the position of double bonds in dietary fatty acids, as well as the quantity of dietary fat, may have a significant effect on the regulation of oxidative and thermogenic conditions in vivo.
Highlights
Obesity, which is a condition of excessive adipose tissue accumulation [1], increases the risk of metabolic disorders, such as type 2 diabetes, dyslipidemia, and cardiovascular diseases [2].Consumption of high fat diet contributes to obesity development because fatty acids increase caloric density of diets, and dietary fatty acids and their metabolites modulate the transcription of lipogenic and lipolytic genes [3]
Four-week-old male C57BL/6J mice were purchased from the Jackson Laboratory and were maintained on a chow diet for four days before being assigned to one of five diet groups; control diet containing 5.6% kcal fat from lard and 4.4% kcal fat from soybean oil (CON) or high-fat diets (HFD) containing 25% kcal from lard and 20% kcal fat from shea butter (SHB; STA rich), olive oil (OO; OLA rich), safflower oil (SFO; LNA rich), or soybean oil (SBO; mixture of OLA, LNA, and ALA)
It is possible that the downregulation of thermoregulatory genes, including Ucp1, Pgc1a, and Adrb3 in epididymal WAT (eWAT) of the SHB group is partly responsible for the higher weight gain in this group
Summary
Obesity, which is a condition of excessive adipose tissue accumulation [1], increases the risk of metabolic disorders, such as type 2 diabetes, dyslipidemia, and cardiovascular diseases [2]. Consumption of high fat diet contributes to obesity development because fatty acids increase caloric density of diets, and dietary fatty acids and their metabolites modulate the transcription of lipogenic and lipolytic genes [3]. Fatty acids differentially regulate metabolism and exert divergent effects on obesity occurrence. As compared to monounsaturated (MUFA) or saturated fatty acids (SFA), polyunsaturated fatty acids (PUFA) are potent suppressors of transcription of lipogenic genes through peroxisome proliferator-activated receptors (PPAR) mediated mechanisms [4], as antagonists of liver X receptors (LXR) [5], or by downregulating the expression of the sterol regulatory element-binding proteins (SREBP) [6].
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