Adiposidad visceral y resistencia insulínica: rol de la AMPK
DOI:
https://doi.org/10.14409/fabicib.v23i0.8367Keywords:
sucrose-rich diet, visceral adiposity, insulin resistance, AMPKAbstract
Introduction: the adipose tissue dysfunction constitutes a central point in the development of complications associated with the Metabolic Syndrome. AMP-activated protein kinase (AMPK) is considered a cellular metabolic sensor, with an important role in the regulation of the metabolic activity of white adipose tissue.
Objectives: to evaluate the effects of the chronic administration of a sucrose rich diet on some mechanisms involved in adipose tissue dysfunction and insulin resistance.
Materials and methods: male Wistar rats received a reference diet (DR) or a sucrose-rich diet (SRD) for six months. At the end of the experimental period, the anthropometric parameters and visceral adiposity index were analyzed. In epididymal adipose tissue: triglyceride content, carnitine palmitoyl transferase enzymes activities (CPT1, CPT2 and totalCPT) and protein mass levels of AMPK and AMPKp. Serum levels of triglycerides, free fatty acid, glucose, insulin and TNFα were determined. Insulin sensitivity was measured by the euglycemic-hyperinsulinemic clamp technique.
Results: in insulin resistant dyslipidemic rats fed with SRD presented a significant increase in anthropometric parameters (body weight, CT, CA1 and 2), BMI and visceral adiposity index. In the epididymal adipose tissue, an increase in the content of triglycerides was observed, without changes in the transport of fatty acids (estimated by the measurement of the CPT activity). In addition, a decrease in the protein mass of the phosphorylated AMPK was observed that correlated with the high serum levels of TNFα.
Conclusions: the findings provide new mechanisms that involve AMPK in visceral adipose tissue dysfunction in insulin-resistant dyslipidemic rats.