Polyunsaturated fatty acids of marine origin induce adiponectin in mice fed a high-fat diet

Abstract

Aims/hypothesis: Diets rich in n-3 polyunsaturated fatty acids, namely eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), protect against insulin resistance and obesity in rodents and increase insulin sensitivity in healthy humans. We tested whether the anti-diabetic effects of EPA and DHA involve enhanced production of the endogenous insulin sensitiser, adiponectin. Methods: We studied the effects, in an obesity-promoting high-fat diet, of partial replacement of vegetable oils by EPA/DHA concentrate (6% EPA, 51% DHA) over a 5-week period in adult male C57BL/6J mice that either had free access to food or had their food intake restricted by 30%. At the end of the treatment, systemic markers of lipid and glucose metabolism and full-length adiponectin and leptin were measured. Adiponectin (Adipoq) and leptin (Lep) gene expression in dorsolumbar and epididymal white adipose tissue (WAT) and isolated adipocytes was quantified and adipokine production from WAT explants evaluated. Results: In mice with free access to food, plasma triacylglycerols, NEFA, and insulin levels were lower in the presence of EPA/DHA, while glucose and leptin levels were not significantly altered. Food restriction decreased plasma triacylglycerols, glucose, insulin and leptin, but not adiponectin. EPA/DHA increased plasma adiponectin levels, independent of food intake, reflecting the stimulation of Adipoq expression in adipocytes and the release of adiponectin from WAT, particularly from epididymal fat. Expression of Lep and the release of leptin from WAT, while being extremely sensitive to caloric restriction, was unaltered by EPA/DHA. Conclusions/interpretation: Intake of diets rich in EPA and DHA leads to elevated systemic concentrations of adiponectin, largely independent of food intake or adiposity and explain, to some extent, their anti-diabetic effects.

Negative association between plasma levels of adiponectin and polychlorinated biphenyl 153 in obese women under non-energy-restrictive regime

“…18 Furthermore, n-3 polyunsaturated fatty acids downregulate phenobarbital-induced CYP 2B expression, 19 whereas they upregulate adiponectin and improve glucose homeostasis. 20 Therefore, a hypothesis may be tested whether PCB 153 downregulates adiponectin through induction of CYP 2B, or whether adiponectin and CYP 2B represent two independent targets for PCB 153 in adipose tissue. Further studies should be performed to reveal (1) whether it was the negative energy balance or the new achieved lighter body weight in itself that resulted in the disappearance of negative correlation between adiponectin Figure 1 Negative correlation between plasma levels of total immunoreactive adiponectin and PCB 153 in OB.…”

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

“…Blood glucose was measured by calibrated glucometers (LifeScan, Milpitas, CA, USA). Total adiponectin was measured by ELISA [31] (R&D Systems, Abingdon, UK). Distribution of adiponectin multimeric complexes was determined using western blotting [33].…”

“…In spite of the differences in the ability of TZDs and n-3 LC-PUFA to reverse IGT, both types of compounds reduce adipose tissue inflammation [24,30], one of the key factors contributing to the development of insulin resistance in obesity, while also increasing adiponectin [12,15,24,25,31,32].…”

Beneficial effects of long-chain n-3 fatty acids included in an energy-restricted diet on insulin resistance in overweight and obese European young adults

“…Based on this evidence, it has been hypothesised that possible protective effects of EPA and DHA may involve induction of adiponectin. In animal research, the intake of diets rich in EPA and DHA (5.3% of total energy intake) leads to elevated systemic concentrations of adiponectin, largely independent of food intake or adiposity [24].…”