Relationship of visceral adipose tissue and glucose disposal is independent of sex in black NIDDM subjects

1997 ◽  
Vol 273 (2) ◽  
pp. E425-E432 ◽  
Author(s):  
M. A. Banerji ◽  
J. Lebowitz ◽  
R. L. Chaiken ◽  
D. Gordon ◽  
J. G. Kral ◽  
...  

To determine the interrelationship among insulin action, total or regional adiposity, and sex, we measured insulin-mediated glucose disposal by the euglycemic insulin clamp and adipose distribution using computed axial tomography (22 scans) in 32 black men and 20 black women with non-insulin-dependent diabetes mellitus (age 48 +/- 9 and 54 +/- 9 yr, body mass index 26.3 +/- 2.3 and 27.2 +/- 2.6 kg/m2, respectively). Women had approximately 80% more total and subcutaneous fat volume than men (31.8 +/- 8.3 vs. 18.6 +/- 6.1 and 28.5 +/- 7.3 vs. 14.7 +/- 4.6 liters) and less muscle volume (22.9 +/- 3.7 vs. 35.1 +/- 3.8 liters). Visceral fat volume did not differ between men and women (3.49 +/- 1.65 vs. 2.96 +/- 1.22 liters). Despite these body composition differences, an inverse nonlinear relationship existed between glucose disposal and visceral fat independent of sex (r = -0.58, P < 0.0001; men r = -0.60 and women r = -0.59; the slope and intercept were not different in men and women). Visceral fat explained a significant portion (34%) of variance in insulin-mediated glucose disposal, whereas total or subcutaneous fat and sex did not. Visceral fat appears to affect glucose disposal over a restricted range (up to approximately 2.5 l/m2 body surface area.

1992 ◽  
Vol 82 (5) ◽  
pp. 565-571 ◽  
Author(s):  
G. R. Fulcher ◽  
M. Walker ◽  
C. Catalano ◽  
M. Farrer ◽  
K. G. M. M. Alberti

1. Increased rates of fatty acid oxidation are frequently observed in patients with non-insulin-dependent diabetes mellitus and may contribute to hyperglycaemia by both decreasing peripheral glucose disposal and, more importantly, by increasing the rate of gluconeogenesis and therefore hepatic glucose output. Despite this relationship between lipid and carbohydrate metabolism, fasting glucose concentrations do not fall acutely in patients with non-insulin-dependent diabetes mellitus when plasma non-esterified fatty acid concentrations and lipid oxidation rates are decreased, questioning the importance of this interaction to glycaemic control. We have therefore measured the acute changes that occur 120–150 min after administration of 500 mg of the anti-lipolytic agent acipimox in eight non-obese male patients with non-insulin-dependent diabetes mellitus. 2. After administration of acipimox, lipolysis was inhibited as reflected by lower plasma non-esterified fatty acid (0.05 ± 0.02 versus 0.55 ± 0.05 mmol/1, P < 0.001) and blood glycerol (8 ± 1 versus 56 ± 8 μmol/l, P < 0.001) concentrations. The lipid oxidation rate was decreased (0.63 ± 0.05 versus 1.02 ± 0.08 mg min−1 kg−1, P < 0.001), whereas there was a significant increase in the carbohydrate oxidation rate (1.93 ± 0.17 versus 1.22 ± 0.18 mg min−1 kg−1, P = 0.02). In addition, in the lipolysis-suppressed patients, there was a significant increase in serum cortisol (329 ± 47 versus 196 ± 43 nmol/l, P=0.03), serum growth hormone (5.44 ± 2.1 versus 0.6 ± 0.2 ng/ml, P=0.04), plasma glucagon (12 ± 2.5 versus 8.2 ± 2.0 ng min−1 ml−1, P = 0.005), plasma noradrenaline (1.82 ± 0.26 versus 1.39 ± 0.21 nmol/l, P=0.004) and adrenaline (0.32 ± 0.08 versus 0.20 ± 0.05 nmol/l, P=0.04) concentrations compared with control. Despite this marked hormonal response, there was no difference in hepatic glucose output, fasting blood glucose concentration or peripheral glucose disposal, although non-oxidative glucose disposal was less after acipimox (0.16 ± 0.16 versus 0.74 ± 0.20 mg min−1 kg−1, P=0.05). 3. We conclude that an acute decrease in fatty acid oxidation results in a switch to oxidation of glucose at the expense of glycogen stores, but apparently does not increase peripheral glucose uptake. Hepatic glucose output and fasting blood glucose concentration are maintained by an acute counter-regulatory response which presumably increases glycogen breakdown. Inhibitors of lipolysis and lipid oxidation are therefore more likely to lower fasting blood glucose concentration in the glycogen-depleted state.


2013 ◽  
Vol 31 (15_suppl) ◽  
pp. e14665-e14665
Author(s):  
Yuji Miyamoto ◽  
Yasuo Sakamoto ◽  
Masayuki Watanabe ◽  
Hideo Baba

e14665 Background: A large amount of visceral adipose tissue might be correlated with high VEGF levels and with resistance to bevacizumab-based regimens in metastasic colorectal cancer (mCRC). The aim is to evaluate that abdominal obesity can be a predictive marker of response to bevacizumab-based therapy in mCRC. Methods: From January 2005 to December 2010, we performed a retrospective analysis of 74 consecutive patients with mCRC received bevacizumab-based first line treatment. Pretreatment CT was used to measure visceral fat volume (VFV), subcutaneous fat volume (SFV) an waist circumference (WC) in 74 patients with mCRC who received bevacizumab-based first-line treatment (bevacizumab group, n=37) or chemotherapy alone (chemotherapy group, n=37). Associations linkingVFV, SFV and WC to tumor response, progression free survival (PFS) and overall survival (OS) were evaluated. For all analyses, VFV, SFV and WC were dichotomized using the median as the cut-off point. Results: In the bevacizumab group, median follow-up lasted for 25 months (7-47). VFV, SFV and WC values were not associated with response or OS. PFS was shorter in patients with high VFV (12.8 vs 7.7 months; p=0.04). By multivariate analysis, high VFA was independently associated with PFS (HR=4.32, p=0.045). In the chemotherapy group, median follow-up lasted for 26 months (2-68). VFV, SFV and WC were not associated with response, PFS or OS. Conclusions: Visceral fat volume plays a role of predictive marker of PFS to bevacizumab-based therapy for Japanese patients with mCRC.


2019 ◽  
Vol 37 (15_suppl) ◽  
pp. e17031-e17031
Author(s):  
Stuart-Allison Moffat Staley ◽  
Katherine Tucker ◽  
Jorge Oldan ◽  
Dominic T. Moore ◽  
Meredith Newton ◽  
...  

e17031 Background: Obesity has been linked to worse outcomes in epithelial ovarian cancer (EOC), due to underlying metabolic dysfunction. Visceral fat (i.e. central obesity) compared to subcutaneous fat is more metabolically active and has been linked to higher rates of obesity-related comorbidities such as hypertension and diabetes, but less is known of the impact of increased visceral adiposity on EOC outcomes. Thus, our goal was to evaluate if visceral adiposity, as determined by computed tomography (CT) morphometric measurements, was associated with worse outcomes in EOC patients undergoing platinum and taxane-based chemotherapy. Methods: EOC patients diagnosed between 12/2004 and 5/2016 who received neoadjuvant or adjuvant treatment with platinum and taxane-based chemotherapy were included. Data on age, stage, grade, histology, BMI, comorbidities, treatment approaches and outcomes were collected. CT images closest to the time of diagnosis were retrospectively evaluated for mid-waist visceral fat volume (VFV), mid-waist subcutaneous fat volume (SFV) and the ratio of mid-waist VFV/SFV. Visceral adiposity is commonly defined as a VFV/SFV ≥ 0.4. Cox regression models were used to analyze time-to-event outcomes. Results: Two hundred fifty-eight EOC patients were evaluated. Seventy-five percent of patients were diagnosed with Stage III or IV disease, with high grade serous as the most common histology (72%). Median age at diagnosis was 62.4 years. Approximately 65% were obese; the median BMI was 26.8 (IQR 23.1 – 32.6). The median VFV/SFV ratio was 0.46 (IQR 0.32 – 0.70). Patients were categorized into those with a VFV/SFV ratio greater than 0.4 or a ratio less than 0.4. When comparing these two groups, there was no difference in progression free survival (PFS) for women with a VFV/SFV ratio greater or less than 0.4 (p = 0.22). However, a VFV/SFV ratio of greater than 0.4 was associated with worse overall survival (OS) (p = 0.01). Conclusions: We found that visceral adiposity, defined as a VFV/SFV ratio greater than 0.4, appeared to be associated with decreased OS, but not PFS. These findings suggest that body fat distribution may be an important prognostic factor for EOC and should be further explored as we expect the obesity epidemic to continue and influence EOC oncologic outcomes.


2006 ◽  
Vol 100 (5) ◽  
pp. 1584-1589 ◽  
Author(s):  
Valerie B. O’Leary ◽  
Christine M. Marchetti ◽  
Raj K. Krishnan ◽  
Bradley P. Stetzer ◽  
Frank Gonzalez ◽  
...  

Exercise improves glucose metabolism and delays the onset and/or reverses insulin resistance in the elderly by an unknown mechanism. In the present study, we examined the effects of exercise training on glucose metabolism, abdominal adiposity, and adipocytokines in obese elderly. Sixteen obese men and women (age = 63 ± 1 yr, body mass index = 33.2 ± 1.4 kg/m2) participated in a 12-wk supervised exercise program (5 days/wk, 60 min/day, treadmill/cycle ergometry at 85% of heart rate maximum). Visceral fat (VF), subcutaneous fat, and total abdominal fat were measured by computed tomography. Fat mass and fat-free mass were assessed by hydrostatic weighing. An oral glucose tolerance test was used to determine changes in insulin resistance. Exercise training increased maximal oxygen consumption (21.3 ± 0.8 vs. 24.3 ± 1.0 ml·kg−1·min−1, P < 0.0001), decreased body weight ( P < 0.0001) and fat mass ( P < 0.001), while fat-free mass was not altered ( P > 0.05). VF (176 ± 20 vs. 136 ± 17 cm2, P < 0.0001), subcutaneous fat (351 ± 34 vs. 305 ± 28 cm2, P < 0.03), and total abdominal fat (525 ± 40 vs. 443 ± 34 cm2, P < 0.003) were reduced through training. Circulating leptin was lower ( P < 0.003) after training, but total adiponectin and tumor necrosis factor-α remained unchanged. Insulin resistance was reversed by exercise (40.1 ± 7.7 vs. 27.6 ± 5.6 units, P < 0.01) and correlated with changes in VF ( r = 0.66, P < 0.01) and maximal oxygen consumption ( r = −0.48, P < 0.05) but not adipocytokines. VF loss after aerobic exercise training improves glucose metabolism and is associated with the reversal of insulin resistance in older obese men and women.


Circulation ◽  
1995 ◽  
Vol 92 (7) ◽  
pp. 1770-1778 ◽  
Author(s):  
Melissa A. Austin ◽  
Leena Mykkänen ◽  
Johanna Kuusisto ◽  
Karen L. Edwards ◽  
Carrie Nelson ◽  
...  

1995 ◽  
Vol 269 (4) ◽  
pp. E745-E752 ◽  
Author(s):  
T. W. Balon ◽  
J. L. Gu ◽  
Y. Tokuyama ◽  
A. P. Jasman ◽  
J. L. Nadler

We examined the effects of a magnesium-supplemented (Mg-S) diet in the male obese Zucker diabetic fatty rat, a model of non-insulin-dependent diabetes mellitus (NIDDM). Obese rats were maintained on either a control (0.20% Mg) or magnesium-supplemented (Mg-S; 1% Mg) diet for 6 wk beginning at 6 wk of age. The rats maintained on the Mg-S diet had markedly lower fasting and fed-state blood glucose concentrations and an improved glucose disposal. By 12 wk of age, all of the eight animals on the control diet became diabetic, whereas diabetes developed in only one of eight animals on the Mg-S diet. Insulin and C-peptide concentrations, in addition to pancreatic GLUT-2 and insulin mRNA expression, were higher in the male obese Mg-S rats than in their control-fed counterparts. A subgroup of rats on the control diet with established diabetes was switched to a Mg-S diet for an additional 4 wk. The Mg-S diet did not reverse diabetes once already established. These data indicate that an increased dietary Mg intake in male obese rats prevents deterioration of glucose tolerance, thus delaying the development of spontaneous NIDDM.


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