Fructose-rich diet-induced abdominal adipose tissue endocrine dysfunction in normal male rats

Abstract

We have currently studied the changes induced by administration of a fructose-rich diet (FRD) to normal rats in the mass and the endocrine function of abdominal (omental) adipose tissue (AAT). Rats were fed ad libitum a standard commercial chow and tap water, either alone (control diet, CD) or containing fructose (10%, w/vol) (FRD). Three weeks after treatment, circulating metabolic markers and leptin release from adipocytes of AAT were measured. Plasma free fatty acids (FFAs), leptin, adiponectin, and plasminogen activator inhibitor-1 (PAI-1) levels were significantly higher in FRD than in CD rats. AAT mass was greater in FRD than in CD rats and their adipocytes were larger, they secreted more leptin and showed impaired insulin sensitivity. While leptin mRNA expression increased in AAT from FRD rats, gene expression of insulin receptor substrate, IRS1 and IRS2 was significantly reduced. Our study demonstrates that administration of a FRD significantly affects insulin sensitivity and several AAT endocrine/metabolic functions. These alterations could be part of a network of interacting abnormalities triggered by FRD-induced oxidative stress at the AAT level. In view of the impaired glucose tolerance observed in FRD rats, these alterations could play a key role in both the development of metabolic syndrome (MS) and beta-cell failure.

Rat liver uncoupling protein 2: Changes induced by a fructose-rich diet

“…As previously reported, our FRD-fed rats presented insulin resistance, as demonstrated by hyperinsulinemia with normoglycemia and the HOMA-IR index, significantly increased serum triglyceride levels, impaired glucose tolerance and oxidative stress markers (Alzamendi et al, 2009;Francini et al, 2009Francini et al, , 2010Rebolledo et al, 2008).…”

“…Although the underlying mechanism responsible for the detrimental effects of fructose-rich diets (FRD) is not quite clear, it is known that such diets promote an increase of glycoxidative stress (Busserolles et al, 2002;Girard et al, 2006;Lange et al, 1980;Thirunavukkarasu et al, 2004). In fact, we have previously demonstrated that short-term administration of a FRD to normal rats induces significant changes in many metabolic, endocrine and glycoxidative stress markers (Alzamendi et al, 2009;Francini et al, 2009Francini et al, , 2010Rebolledo et al, 2008).…”

Quercetin attenuates high fructose feeding-induced atherosclerosis by suppressing inflammation and apoptosis via ROS-regulated PI3K/AKT signaling pathway

“…Previous studies have indicated that the PI3K/AKT pathway is associated with ROS production [26,38]. The PI3K/AKT pathway is included in protecting against not only ROS production but also apoptotic insults [39]. It has been suggested that quercetin showed anti-disease and anti-cancer activity via inhibiting ROS directly [40].…”

Excess fructose intake‐induced hypertrophic visceral adipose tissue results from unbalanced precursor cell adipogenic signals

“…In these animals, we also recorded a marked increase in visceral adipose tissue (VAT) mass and impairment of its metabolic and endocrine functions [1][2][3].…”