Antioxidant treatment prevents the development of fructose-induced abdominal adipose tissue dysfunction

Abstract

In the present study, we tested the effect of OS (oxidative stress) inhibition in rats fed on an FRD [fructose-rich diet; 10% (w/v) in drinking water] for 3 weeks. Normal adult male rats received a standard CD (commercial diet) or an FRD without or with an inhibitor of NADPH oxidase, APO (apocynin; 5 mM in drinking water; CD-APO and FRD-APO). We thereafter measured plasma OS and metabolic-endocrine markers, AAT (abdominal adipose tissue) mass and cell size, FA (fatty acid) composition (content and release), OS status, LEP (leptin) and IRS (insulin receptor substrate)-1/IRS-2 mRNAs, ROS (reactive oxygen species) production, NADPH oxidase activity and LEP release by isolated AAT adipocytes. FRD-fed rats had larger AAT mass without changes in body weight, and higher plasma levels of TAG (triacylglycerol), FAs, TBARS (thiobarbituric acid-reactive substance) and LEP. Although no significant changes in glucose and insulin plasma levels were observed in these animals, their HOMA-IR (homoeostasis model assessment of insulin resistance) values were significantly higher than those of CD. The AAT from FRD-fed rats had larger adipocytes, higher saturated FA content, higher NADPH oxidase activity, greater ROS production, a distorted FA content/release pattern, lower insulin sensitivity together with higher and lower mRNA content of LEP and IRS-1-/2 respectively, and released a larger amount of LEP. The development of all the clinical, OS, metabolic, endocrine and molecular changes induced by the FRD were significantly prevented by APO co-administration. The fact that APO treatment prevented both changes in NADPH oxidase activity and the development of all the FRD-induced AAT dysfunctions in normal rats strongly suggests that OS plays an important role in the FRD-induced MS (metabolic syndrome) phenotype.

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

“…Bcl-2 has been well known as an effective anti-apoptotic factor, leading to Bax inactivation and reliving mitochondria. However, Bcl-2 function loss is a major cause for Caspase-3 activation, resulting in apoptosis [41]. These results above in vivo indicated that quercetin showed effects on enhancing AKT activity.…”

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

“…We still do not know the precise mechanism that triggers this pro-/anti-adipogenic balance in FRD rats. It is tempting to speculate that the general oxidative stress (TBARS) and local oxidative stress (VAT) [3] present in FRD animals could be one such trigger. This state of FRD-induced high oxidative stress could in turn decrease sirtuin-1 production [25], a NAD + -dependent histone deacetylase that represses PPARc expression [26] and thus inhibits adipogenesis.…”

“…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].…”

“…the unhealthy expansion) of its cells [6] and an increased peripheral/VAT oxidative stress [3]. However, the underlying mechanism whereby the FRD induces this selective adipocyte hypertrophy rather than its hyperplasia remains unknown.…”

“…As described previously [1][2][3], normal adult male SpragueDawley rats (aged 60 days) were kept in a temperaturecontrolled environment under a 12 : 12 h light/dark cycle at at 23 ºC. Animals were fed a Purina (Ganave SA, Pilar, Argentina) commercial rat chow ad libitum for 3 weeks and either tap water only (conventionally designated as the CD) or with the addition of 10% fructose (w/v) in drinking water (conventionally designated as the FRD).…”