Abstract
The aim of this research was to estimate the preventive effects of filbertone, the main flavor compound in hazelnuts, on lipid accumulation in the adipose tissue of mice fed a high-fat diet (HFD) and to reveal the underlying molecular mechanisms. Male C57BL/6N mice were fed chow, a HFD, or a 0.025% filbertone-supplemented HFD for 14 weeks. We found that filbertone supplementation resulted in significant reductions in body weight gain and lipid accumulation in adipose tissue, with parallel improvements in plasma lipid levels (triglycerides, total cholesterol, and free fatty acids) and proinflammatory cytokines (interleukin 6 (IL-6) and tumor necrosis factor alpha (TNF-α)). Molecular analysis revealed that filbertone treatment led to reprogramming of metabolic signatures in the cyclic adenosine monophosphate (cAMP) pathway. Filbertone supplementation significantly increased the cAMP level and increased downstream protein kinase A catalytic subunit (PKA) signaling in mouse adipose tissue. The mRNA level of adipogenesis-related genes was downregulated in the adipose tissue of filbertone-fed mice compared to control mice fed the HFD alone. Furthermore, filbertone treatment elevated the expression of thermogenic genes in mouse adipose tissue. Filbertone reduced intracellular lipid accumulation and increased the oxygen consumption rate in 3T3-L1 cells and these filbertone-induced changes were abrogated by the adenylate cyclases (ADCY) inhibitor. Taken together, our results suggest that the beneficial effects of filbertone on lipid accumulation may be associated with the activation of cAMP signaling.
Highlights
Obesity is a chronic condition of energy imbalance whereby a long-term overload of energy intake over expenditure results in the stocking of that excess energy in white adipose tissue (WAT) [1]
Mice fed the filbertone for 14 weeks showed significant reductions in final body weight and body weight gain as compared to control mice fed high-fat diet (HFD) alone, without changes in food intake (Figure 1a–c)
We examined adipocyte size to determine whether filbertone inhibits lipid storage in adipose tissues
Summary
Obesity is a chronic condition of energy imbalance whereby a long-term overload of energy intake over expenditure results in the stocking of that excess energy in white adipose tissue (WAT) [1]. WAT is well established to be predisposed to the development of dyslipidemia, insulin resistance, diabetes, and accelerated macrovascular disease. The existence of fat at ectopic sites, either alone or in relation to elevated visceral adiposity, is an independent determinant of the development of a large number of metabolic diseases [3,4]. Signaling by β-adrenergic receptors elicits increased cAMP levels and subsequent lipolysis in WAT and brown adipose tissue (BAT); mice lacking all three β-adrenergic receptors (β1-, β2-, and β3-AR) have a decreased metabolic rate and are mildly obese
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