Differential effects of high MUFA with high or low P/S ratio (polyunsaturated to saturated fatty acids) on improving hepatic lipolytic enzymes and mediating PPARγ related with lipoprotein lipase and hormone-sensitive lipase of white adipose tissue in diet-induced obese hamster

Abstract

Objective: The aim of this study was to assess the relationship between high monounsaturated fatty acids (MUFAs) with different levels of polyunsaturated-to-saturated fatty acid (P/S) ratios and body fat loss in diet-induced obesity (DIO) models. Design: Male Golden Syrian hamsters were randomly assigned to the control group (n ¼ 12) and obesity group (n ¼ 24) for 4 weeks of the high-fat DIO period; afterward, six hamsters from each group were killed. The remaining control hamsters were still fed a low-fat diet. For an additional 8 weeks, the remaining obesity hamsters were switched to a low-fat diet and subdivided into three subgroups (n ¼ 6/group): the obesity-control (ObC) group, high MUFA with high P/S ratio oil (HMHR) group and olive oil (OO) group. Serum insulin and leptin concentrations were measured, and hepatic fatty acid metabolic enzymes and adipose differentiation markers were determined using enzyme activities analysis, western blot and semiquantification reverse-transcription PCR. Results: No difference was observed in the mean energy intake through all study periods. After the DIO period, the obesity group increased in weight gain and epididymal fat weight compared with the control group. DIO hamsters in the HMLR group had significant reductions in white adipose tissue deposition and plasma leptin levels, suppression in adipose peroxisome proliferator-activated receptor-g (PPARg) and lipoprotein lipase (LPL) mRNA expressions and increases in hepatic acyl-CoA oxidase and carnitine palmitoyltransferase-I activities and mRNA levels compared with those in the ObC group. The HMHR group had upregulated phosphorylation of hormone-sensitive lipase (HSL) relative to total HSL protein levels compared with the OO group. However, the OO group had significantly elevated hepatic de novo lipogenesis compared with the HMHR group. Conclusions: HMHR seemed to be beneficial in depleting white adipose tissue accumulation by decreasing adipose PPARg and LPL mRNA expressions and mediating phosphorylation of HSL, and by improving hepatic lipolytic enzyme activities and mRNA expressions involved in b-oxidation in DIO hamsters.

Cellular mechanisms regulating fuel metabolism in mammals: Role of adipose tissue and lipids during prolonged food deprivation

“…As carbohydrate stores are depleted, defined mechanisms shift metabolism to reliance on lipid oxidation, with a small degree of protein catabolism, until either a food source is found or the organism enters irreversible terminal cachexia and succumbs. Though the characterization of the three phases was a substantial addition to our understanding of starvation metabolism, there has been substantial work demonstrating that the regulation of substrate utilization goes beyond the hormone-mediated hydrolysis of available substrate [36, 46, 72–74]. Lipids exhibit substantial control over metabolism through transcription regulation and through β-oxidation [72, 73, 75, 76], and increase in circulation as a result of food deprivation [9].…”

“…PUFA inhibit sterol regulatory element-binding protein (SREBP) activity via deactivation of hepatic LXR, which impedes lipogenesis [55]. Monounsaturated fatty acids (MUFA) promote lipolysis through inhibition of PPARγ, but do not significantly affect oxidation in rats and hamsters [72, 74]. Saturated fatty acids (SFA) increase low-density lipoprotein (LDL) production, but have also been suggested to contribute to FA chain elongation and to increase the expression of genes involved in hepatic de novo lipogenesis in mice [81–83].…”

Effect of high-fat diets on body composition, lipid metabolism and insulin sensitivity, and the role of exercise on these parameters

“…However, when PUFA were added to a high-MUFA diet (high PUFA/SFA ratio) for 8 weeks, the expression and activity of hormone-sensitive lipase (HSL) was upregulated and adipose tissue peroxisome proliferatoractivated gamma (PPARγ) was reduced when compared to a high-MUFA diet, which significantly elevated de novo hepatic lipogenesis (18). Studies comparing the effects of safflower oil (omega 6 FA) versus beef tallow (SFA) in rats reported that the latter group had a higher fat content in the carcass, decreased sympathetic activity and a lower thermogenic effect (19).…”

“…While SFA play a negative role in body composition, unsaturated fatty acids seem to have the opposite effect through the following mechanisms: decreased energy intake and/or increased energy expenditure through the activation of mitochondrial uncoupling proteins (19); reduced lipid uptake by white adipocytes by suppression of lipoprotein lipase (25); increased lipid catabolism enhancing FA oxidation (β-oxidation) (25); decreased triacylglycerol synthesis through inhibition of enzymes such as fatty acid synthase (FAS) and stearoyl-CoA desaturase-1 (26); decreased expression of transcriptional factors and genes involved in adipose tissue metabolism (18); PPARs are transcriptional factors of the nuclear receptors family, with a key role in controlling lipid metabolism, adipocyte differentiation and lipid storage. There are two important classes of PPARs: PPARα and PPARγ.…”

Oral Administration of Alkylglycerols Differentially Modulates High-Fat Diet-Induced Obesity and Insulin Resistance in Mice

“…In metabolic experiments, rats fed saturated fatty acids had higher triacylglycerol, cholesterol, and low-density lipoprotein cholesterol, whereas rats fed unsaturated fatty acids had lower triacylglycerol, cholesterol, and low-density lipoprotein cholesterol as compared with control rats [41, 42]. Moreover, the increased ratio of P/S (polyunsaturated/saturated) fatty acids was beneficial in depleting white adipose tissue accumulation and improved the metabolic status in diet-induced obese hamster [43]. The controlled clinical trials have also indicated that replacing saturated fat with unsaturated fat was more effective in lowering risk of metabolic disorder than simply reducing total fat consumption [44, 45].…”