Περίληψη:
The aim of this review is to summarize the mechanisms underlying insulin
resistance in morbid obesity. Glucose regulation by insulin depends on
the suppression of endogenous glucose production and stimulation of
glucose disposal. In morbid obesity, glucose production by the liver is
increased. Moreover, the sensitivity of glucose metabolism to insulin is
impaired both in muscle (due to defects in insulin-stimulated glucose
utilization and decreased blood flow) and in adipose tissue (due to
decreased blood flow). However, recent studies suggest that expanded
total fat mass becomes a major consumer of glucose providing a sink for
glucose and compensating for insulin resistance. Metabolism and immunity
are closely linked. Bearing in mind the crosstalk between inflammatory
pathways and the insulin signaling cascade, adipose tissue derived
cytokines may represent a link between inflammation and metabolic
signals and mediate, at least in part, insulin resistance. Adipose
tissue plays a crucial role by buffering daily influx of dietary fat,
suppressing the release of non-esterified fatty acids into the
circulation and increasing triacylglycerol clearance. However, in morbid
obesity there is an impairment of the normal ability of adipose tissue
to buffer fatty acids, despite hyperinsulinemia. Lipotoxicity gradually
impairs insulin action in the liver and muscle, aggravating insulin
resistance.
Συγγραφείς:
Mitrou, Panayota
Raptis, Sotirios A.
Dimitriadis, George
