The relationship between regional abdominal fat distribution and both insulin resistance and subclinical chronic inflammation in non-diabetic adults

Abstract

ObjectiveObesity is associated with a high risk of insulin resistance (IR) and its metabolic complications. It is still debated that distributions of adipose tissue relate to an excess risk of IR and chronic inflammation in different race. This study was designed to examine the relation between insulin sensitivity, chronic inflammation and central fat distribution in non-diabetic volunteers in Taiwanese.MethodsThere were 328 volunteers without family history of diabetes mellitus and with normal oral glucose tolerance test enrolled. Total body fat and abdominal fat were measured. Abdominal fat was categorized into intraperitoneal (IP), retroperitoneal (RP) and subcutaneous (SC) fat. The IR index was estimated by homeostatic model assessment. Five inflammatory markers: adiponectin, leptin, tumor necrosing factor-α (TNF-α), resistin and high sensitive CRP (hs-CRP) were measured.ResultsIR was related to IP fat (r = 0.23, p < 0.001), but not RP fat, SC fat or total body fat. After correcting for age and sex, IP fat was the only significant predictor of IR (r2 = 58%, p = 0.001). Leptin showed the strongest relationship with all fat compartments (IP fat: r = 0.44, p = 0.001; RP fat: r = 0.36, p = 0.005, SC fat: r = 0.54, p < 0.001; total body fat: r = 0.61, p < 0.001). The hs-CRP and adiponectin were closely related both to IP (r = 0.29, p = 0.004; r = -0.20, p = 0.046, respectively) and total body fat (r = 0.29, p = 0.004; r = -0.29, p = 0.005, respectively), but not RP, or SC fat. TNF-α and resistin were not correlated to any fat compartment. After correcting for age and sex, leptin variance was mostly explained by SC fat (41.3%), followed by IP fat (33.6%) and RP fat (25.3%). The hs-CRP and adiponectin variance were mostly explained by IP fat (40% and 49% respectively).ConclusionsIP fat is better predictors of IR and subclinical chronic inflammation in Taiwanese adults. A disproportionate accumulation of abdominal fat is associated with increased risk of cardiovascular diseases.

Exercise Dose Effects on Insulin Resistance Indicators in Postmenopausal Women: A Randomized Trial

“…Its production by adipocytes is inhibited by pro-inflammatory factors (e.g., TNF-α, IL-6), hypoxia, and oxidative stress [35]. Low adiponectin concentrations are associated with visceral fatness, which is a risk factor for insulin resistance [36,38]. There are several possible reasons why we did not observe dose effects in intention-to-treat analyses.…”

“…White adipose tissue displays endocrine activity producing adipokines such as resistin, leptin, and adiponectin. In humans, resistin is produced mainly by macrophages and monocytes in response to pro-inflammatory cytokines, and itself is pro-inflammatory [35] although in some studies [9,36] resistin concentrations do not correlate with total body fat. Leptin is an adipocyte-derived hormone involved in energy regulation and is insulin-sensitizing [37].…”

“…Leptin is an adipocyte-derived hormone involved in energy regulation and is insulin-sensitizing [37]. Leptin concentrations correlate positively with total fat [36] and higher levels are believed to reflect leptin resistance. Leptin production is regulated by insulin and glucose metabolism in adipocytes [37] and activity is enhanced with hyperinsulinemia [2].…”

“…2016;6(2): [35][36][37][38][39][40][41][42][43][44][45] high, n = 9 moderate). Moreover, we did not measure peripheral insulin resistance in muscle or fat, which may be relevant to breast cancer etiology.…”

“…Randomized controlled trials (RCTs) designed specifically to evaluate dose Manuscript accepted for publication April 07, 2016 Exercise and Insulin Resistance Indicators J Endocrinol Metab. 2016;6(2): [35][36][37][38][39][40][41][42][43][44][45] effects would inform cancer prevention guidelines. Such trials have been conducted and measured insulin resistance indicators [11][12][13][14][15][16][17][18][19]; however, they were limited for informing postmenopausal breast cancer prevention because they were small [12][13][14], tested lower-intensity exercise [14,15,19] or shorter durations of exercise that may be suboptimal for cancer prevention [15,16], or they did not focus on postmenopausal women [11,13,17].…”