Disease relevance of Abdominal Fat

• CONTEXT: The metabolic syndrome, a concurrence of disturbed glucose and insulin metabolism, overweight and abdominal fat distribution, mild dyslipidemia, and hypertension, is associated with subsequent development of type 2 diabetes mellitus and cardiovascular disease (CVD) [1].
• Increased resistin expression in abdominal fat could explain the increased risk of type 2 diabetes associated with central obesity [2].
• Patients with clinical and subclinical amyloidosis were compared with regard to clinical characteristics and the degree of amyloid deposits in abdominal fat [3].
• The aim of the present study was to examine the combined effects of abdominal fat accumulation and hyperinsulinemia on plasma triglyceride levels among heterozygous patients for familial LPL deficiency [4].
• At 14 wk, plasma leptin concentrations per unit abdominal fat mass were 27% lower in rats fed the high-fat diet (P = 0.058) and there was a significant negative association between leptin concentrations per unit abdominal fat mass and body weight (r = 0.44, P < 0.05) [5].

Psychiatry related information on Abdominal Fat

• The present study was designed to measure interstitial levels of norepinephrine-regulating lipolysis (NE) in subcutaneous abdominal adipose tissue of anorexia nervosa (AN) patients and control subjects under basal conditions and after the local administration of an inhibitor of NE re-uptake, maprotiline [6].
• This study demonstrates a significant relationship between internalized racism and abnormal levels of fasting glucose which may be mediated through abdominal fat [7].

High impact information on Abdominal Fat

• Metformin therapy was associated with a decrease in visceral abdominal fat (VAT; -1115 [819] vs 1191 [699] mm(2); P =.08) and a proportional reduction in subcutaneous abdominal fat (SAT); the VAT-SAT ratio was unchanged in metformin-treated vs placebo-treated patients [8].
• Subcutaneous abdominal adipose tissue of healthy non-obese subjects was microdialyzed with equimolar concentrations of dobutamine (selective beta 1-adrenoceptor agonist), terbutaline (selective beta 2-adrenoceptor agonist), or CGP 12177 (selective beta 3-adrenoceptor agonist) [9].
• The pseudolipolytic effect of clonidine was significantly more pronounced in gluteal as compared with abdominal adipose tissue [10].
• At the end of each period isolated fat cells were prepared from subcutaneous abdominal adipose tissue and incubated in vitro in the absence or presence of adenosine deaminase, either alone or in combination with various lipolytic or antilipolytic hormones and agents [11].
• Visceral abdominal-fat accumulation associated with use of indinavir [12].

Chemical compound and disease context of Abdominal Fat

• While obese women with abdominal (android) fat distribution are more insulin resistant than those with peripheral (gynecoid) obesity, in nonobese women, the relationship between abdominal fat and insulin resistance is unknown [13].
• Adipose cholesterol content did not change in peripheral (arm and leg) biopsy sites but rose significantly in abdominal adipose tissue with weight loss [14].
• Flutamide (Flu)-metformin (Met) with ethinylestradiol-drospirenone is a combination therapy that reduces the total and abdominal fat excess, diminishes the lean mass deficit, and attenuates the dysadipocytokinemia of young and nonobese women with ovarian hyperandrogenism, a variant of polycystic ovary syndrome [15].
• Thus, massive obesity is associated with abnormalities in hormonal balance in gynecologically symptomless women, there being an association between E1, E2, A, LH, cortisol, and relative weight and/or abdominal fat cell size [16].
• Clenbuterol did not change body weight compared with the control group but caused a redistribution of body weight: leg muscle weights increased, and abdominal fat weight decreased [17].

Biological context of Abdominal Fat

• Serum lipids, glucose homeostasis and abdominal adipose tissue distribution in protease inhibitor-treated and naive HIV-infected children [18].
• CONCLUSION/INTERPRETATION: These findings suggest that the missense mutation in the MC4R gene could contribute to the variability in body mass, abdominal fat distribution and leptin concentrations in the general population [19].
• Growth hormone treatment of abdominally obese men reduces abdominal fat mass, improves glucose and lipoprotein metabolism, and reduces diastolic blood pressure [20].
• After 3 months on metformin, all identified aberrations in body composition were attenuated, the most marked changes (P < 0.0001) being a reduction of the excess in abdominal fat and of the deficit in lean body mass; BMI remained unaltered [21].
• By simple linear regression, serum GHBP correlated positively to several indices of adiposity: intraabdominal fat (r = 0.537; P = 0.001), sc abdominal fat (r = 0.680; P < 0.001), BMI (r = 0.483; P = 0.001), W/H ratio (r = 0.452; P = 0.003), total body fat (DEXA scanning; r = 0.503; P = 0.002), and body fat (bioimpedance; r = 0.354; P = 0.023) [22].

Anatomical context of Abdominal Fat

• Role of deep abdominal fat in the association between regional adipose tissue distribution and glucose tolerance in obese women [23].
• The tissues in which DBP gene transcripts were noted by Northern analysis were paralleled at 20 cycles of PCR with liver much greater than kidney, yolk sac, testis, and abdominal fat [24].
• Measurements of glucose disposal rate (GDR) using a euglycemic, hyperinsulinemic glucose clamp; abdominal fat, hepatic fat content, and thigh muscle area using computed tomography; and total body fat and fat-free mass derived from (40)K measurements were performed at baseline and at 6 and 12 months [25].
• In early postmenopausal women the amount of the intra-abdominal fat strongly influences insulin sensitivity and plasma triglyceride levels, whereas plasma free fatty acids are closely related to the amount of the sc abdominal fat [26].
• The concentrations of RU 486 and its demethylated metabolites were determined by RIA in samples of myometrium, abdominal adipose tissue, and serum, which were collected at hysterectomies performed 12-15 h after oral administration of 200 mg RU 486 [27].

Associations of Abdominal Fat with chemical compounds

• Abdominal fat had a significantly stronger relationship with insulin sensitivity than peripheral nonabdominal fat (r2 = 0.79 vs. 0.44), and higher levels were associated with increased fasting nonesterified fatty acids, lipid oxidation, and hepatic glucose output [13].
• In black women, high-density lipoprotein cholesterol was the only measurement adversely affected by abdominal fat; HDL cholesterol was significantly lower in the black UBO group (1.14 +/- 0.05 mM) compared with the black LBO group (1.37 +/- 0.08 mM) [28].
• Both exercise training and food restriction significantly suppressed plasma levels of glucose and insulin and serum levels of triacylglycerol and cholesterol and reduced the accumulation of abdominal fat [29].
• In all patients, the abdominal fat tissue, stained with Congo red, was negative for amyloid deposits [30].
• BACKGROUND: Abdominal fat and circulating triacylglycerols increase with age, which indicates lipid overaccumulation [31].

Gene context of Abdominal Fat

• The direct effect of PRL on the regulation of LPL activity in human abdominal adipose tissue cultured in vitro was investigated [32].
• Waist to hip ratio did not correlate with the levels of circulating hormones or SHBG, but an inverse correlation was found between abdominal fat cell size and A as well as the LH to FSH ratio in the nonhirsute women of the obese group [16].
• In addition, L-PRLR [relative molecular mass (M(r)) 90,000] and I-PRLR (M(r) 50,000) protein expression was detected in human sc abdominal adipose tissue and breast adipose tissue using immunoblot analysis [32].
• We examined the association between the Ala(54)Thr variant in the FABP2 gene and levels of visceral (VAT) and sc (SAAT) abdominal fat in a group of 223 premenopausal African-American (n = 103) and Caucasian (n = 120) women [33].
• Thirteen/fifteen orbital and abdominal fat samples from patients free of GD and TED, measured ex vivo, were negative for TSHR transcripts and two were at the limit of detection [34].

Analytical, diagnostic and therapeutic context of Abdominal Fat

• Insulin sensitivity, measured by intravenous glucose tolerance test, decreased with age (r = -0.32) and was related to abdominal fat content (r = -0.65) [35].
• Lack of amyloid in abdominal fat aspirates from patients undergoing long-term hemodialysis [30].
• DESIGN: We evaluated whole-body glucose metabolism by use of stable-isotope tracer methods and glucose uptake in subcutaneous abdominal adipose tissue by use of arteriovenous balance in 7 lean [58 +/- 2 kg; body mass index (BMI; in kg/m(2)): 21 +/- 5] and 6 abdominally obese (96 +/- 2 kg; BMI: 36 +/- 1) women after 14 and 22 h of fasting [36].
• In the present study, we demonstrated expression of four PRL receptor (PRLR) mRNA isoforms (L, I, S1(a), and S1(b)) in human sc abdominal adipose tissue and breast adipose tissue using RT-PCR/Southern blot analysis [32].
• Subcutaneous abdominal adipose tissue lipolysis was estimated by means of microdialysis combined with measurements of subcutaneous abdominal adipose tissue blood flow (ATBF; (133)Xe washout) [37].

References