Influence of body fat distribution on free fatty acid metabolism in obesity.

Abstract

In order to determine whether differences in body fat distribution result in specific abnormalities of free fatty acid (FFA) metabolism, palmitate turnover, a measure of systemic adipose tissue lipolysis, was measured in 10 women with upper body obesity, 9 women with lower body obesity, and 8 nonobese women under overnight postabsorptive (basal), epinephrine stimulated and insulin suppressed conditions. Results: Upper body obese women had greater (P < 0.005) basal palmitate turnover than lower body obese or nonobese women (2.8±0.2 vs. 2.1±0.2 vs. 1.8±0.2 Mmolt kg lean body mass (LBM)-1 * min-, respectively), but a reduced (P < 0.05) net lipolytic response to epinephrine (59±7 vs. 79±5 vs. 81±7 Mmol palmitate/kg LBM, respectively). Both types of obesity were associated with impaired suppression of FFA turnover in response to euglycemic hyperinsulinemia compared to nonobese women (P < 0.005). These specific differences in FFA metabolism may reflect adipocyte heterogeneity, which may in turn affect the metabolic abberations associated with different types of obesity. These findings emphasize the need to characterize obese subjects before studies.

Non-esterified fatty acids and blood pressure elevation: a mechanism for hypertension in subjects with obesity/insulin resistance?

“…Systolic BP (SBP) increased in both groups, but the increase was significantly greater in subjects with positive than those with no family history of hypertension (1472 vs 1072 mm Hg). 26 Based on such data, it can be speculated that in subjects that typically exhibit chronic NEFA elevation, that is those with central obesity, IR and type II diabetes, [4][5][6] this NEFA increase can be an important factor promoting the development of hypertension in subjects with normal BP levels, or deteriorating BP control in patients with already elevated BP. Further, some of the above data 21,22 support not only a close association between NEFA and BP, but also that this relation could be independent from the degree of IR and other parameters of the metabolic syndrome.…”

“…4 One of the most important factors connecting obesity with the development of related metabolic abnormalities is the elevated release of free or non-esterified fatty acids (NEFAs) from abdominal adipocytes in patients with central obesity, which results in increase in plasma NEFA concentration and turnover. 5,6 NEFAs have been shown to induce both hepatic and peripheral IR, 7,8 to activate apoptotic pathways in pancreatic b cells, 9 to promote endothelial dysfunction 10 and to increase the production of plasminogen activator inhibitor-1. 11 Most importantly, increased NEFA supply of the liver, primarily owing to the incomplete insulin-mediated suppression of lipolysis in this type of subjects, is the initial step for the development of the characteristic lipid disorders of the metabolic syndrome.…”

Upper body fat predicts metabolic syndrome similarly in men and women

“…Three major adipose beds have been identified: gluteofemoral fat (lower body fat), upper body subcutaneous fat and visceral fat. These three beds apparently release NEFA and adipokines at different rates or into different circulatory systems 20, 21, 22, 23. For example, visceral adipose tissue releases NEFA into the portal circulation and delivers them directly into the liver.…”

Exercise training reduces fatty acid availability and improves the insulin sensitivity of glucose metabolism

“…Increased visceral fat may lead to the development of hepatic insulin resistance by increasing release of NEFA into the portal circulation [2], while increased subcutaneous fat may lead to release of more NEFA into the systemic circulation potentially leading to both peripheral and hepatic insulin resistance [3]. Fatty acid flux has been shown to be greater in obese individuals with upper-body obesity than in subjects with lower-body obesity [4,5].…”