Association of comorbid somatic pathology with fat distribution type and body mass index in men

2019 ◽  
Vol 16 (4) ◽  
pp. 328-336 ◽  
Author(s):  
Søren Gullaksen ◽  
Kristian Løkke Funck ◽  
Esben Laugesen ◽  
Troels Krarup Hansen ◽  
Damini Dey ◽  
...  

Objectives: Coronary atherosclerosis in patients with type 2 diabetes mellitus may be promoted by regional fat distribution. We investigated the association between anthropometric measures of obesity, truncal fat mass, epicardial adipose tissue and coronary atherosclerosis in asymptomatic patients and matched controls. Methods: We examined 44 patients and 59 controls [mean (standard deviation) age 64.4 ± 9.9 vs 61.8 ± 9.7, male 50% vs 47%, diabetes duration mean (standard deviation) 7.7 ± 1.5] with coronary computed tomography angiography. Coronary plaques were quantified as total, calcified, non-calcified and low-density non-calcified plaque volumes (mm3). Regional fat distribution was assessed by dual-energy X-ray absorptiometry, body mass index (kg/m2), waist circumference (cm) and epicardial fat volume (mm3). Endothelial function and systemic inflammation were evaluated by peripheral arterial tonometry (log transformed Reactive Hyperemia Index) and C-reactive protein (mg/L). Results: Body mass index and waist circumference ( p < 0.02) were associated with coronary plaque volumes. Body mass index was associated with low-density non-calcified plaque volume after adjustment for age, sex and diabetes status ( p < 0.01). Truncal fat mass ( p > 0.51), waist circumference ( p > 0.06) and epicardial adipose tissue ( p > 0.17) were not associated with coronary plaque volumes in adjusted analyses. Conclusion: Body mass index is associated with coronary plaque volumes in diabetic as well as non-diabetic individuals.


2000 ◽  
Vol 278 (4) ◽  
pp. E700-E706 ◽  
Author(s):  
Daniel E. Flanagan ◽  
Vivienne M. Moore ◽  
Ian F. Godsland ◽  
Richard A. Cockington ◽  
Jeffrey S. Robinson ◽  
...  

Although there is now substantial evidence linking low birthweight with impaired glucose tolerance and type 2 diabetes in adult life, the extent to which reduced fetal growth is associated with impaired insulin sensitivity, defective insulin secretion, or a combination of both factors is not clear. We have therefore examined the relationships between birth size and both insulin sensitivity and insulin secretion as assessed by an intravenous glucose tolerance test with minimal model analysis in 163 men and women, aged 20 yr, born at term in Adelaide, South Australia. Birth size did not correlate with body mass index or fat distribution in men or women. Men who were lighter or shorter as babies were less insulin sensitive ( P = 0.03 and P = 0.01, respectively), independently of their body mass index or body fat distribution. They also had higher insulin secretion ( P = 0.007 and P = 0.006) and increased glucose effectiveness ( P = 0.003 and P = 0.003). Overall glucose tolerance, however, did not correlate with birth size, suggesting that the reduced insulin sensitivity was being compensated for by an increase in insulin secretion and insulin-independent glucose disposal. There were no relationships between birth size and insulin sensitivity or insulin secretion in women. These results show that small size at birth is associated with increased insulin resistance and hyperinsulinemia in young adult life but that these relationships are restricted to the male gender in this age group.


2005 ◽  
Vol 90 (1) ◽  
pp. 32-38 ◽  
Author(s):  
Polyxeni Koutkia ◽  
Bridget Canavan ◽  
Jeff Breu ◽  
Steven Grinspoon

Abstract Prior studies suggest reduced overnight GH secretion in association with excess visceral adiposity among patients with HIV lipodystrophy (LIPO, i.e. with fat redistribution). We now investigate GH responses to standardized GHRH-arginine in LIPO patients (n = 39) in comparison with body mass index- and age-matched control groups [HIV patients without fat distribution (NONLIPO, n = 17)] and healthy subjects (C, n = 16). IGF-I [242 ± 17; 345 ± 38; 291 ± 27 ng/ml (P &lt; 0.05 vs. NONLIPO)] was lowest in the LIPO group. Our data demonstrate failure rates of 18% for the LIPO group vs. 5.9% for the NONLIPO group and 0% for the C group, using a stringent criterion of 3.3 ng/ml for peak GH response to GHRH-arginine (P &lt; 0.05 LIPO vs. C). Using less stringent cutoffs, the failure rate in the LIPO group rises to 38.5% at 7.5 ng/ml. Among the LIPO patients, the peak GH response to GHRH-arginine was significantly predicted by visceral adipose tissue (P = 0.008), free fatty acid (P = 0.04), and insulin level (P = 0.007) in regression modeling controlling for age, body mass index, sc fat area, and triglyceride level. These data demonstrate increased failure rates to standardized stimulation testing with GHRH-arginine in LIPO patients, in association with increased visceral adiposity. The effects of low-dose GH should be assessed in the large subset of LIPO patients with abnormal GH stimulation testing.


2002 ◽  
Vol 87 (8) ◽  
pp. 3984-3988 ◽  
Author(s):  
Valentina Vicennati ◽  
Luana Ceroni ◽  
Lorenza Gagliardi ◽  
Alessandra Gambineri ◽  
Renato Pasquali

Subjects with abdominal obesity are characterized by hyperactivation of the hypothalamic-pituitary-adrenal (HPA) axis. Food intake, particularly at noon, is a well-known inducer of HPA axis activation. Whether obese subjects present an abnormal response to meals containing different macronutrient proportions is at present unknown. Therefore, this study was carried out to investigate the effect of a high-lipid/protein meal (HLP-meal) and a high-carbohydrate meal (HCHO-meal) on the HPA axis activity in women with different obesity phenotypes. Nondepressed, noncomplicated obese (body mass index greater than 28 kg/m2) women with abdominal (A-BFD) (n = 10) and peripheral body fat distribution (P-BFD) (n = 9) and a group of 11 normal-weight controls were investigated in the follicular phase of the menstrual cycle. They were randomly given an 800-kcal HCHO-meal (containing 89% carbohydrates, 11% proteins, 0% lipids), and an 800-kcal HLP-meal (containing 53% lipids, 43% proteins, 4% carbohydrates), which were eaten within 15 min at noon, with an interval of 2 d between each meal. Blood samples for ACTH, cortisol, glucose, and insulin were obtained at 15-min intervals before and after each meal. Baseline hormone and glucose concentrations in the three groups were similar. After the HLP-meal, ACTH tended to similarly but insignificantly increase in all groups, whereas cortisol increased significantly (P &lt; 0.05) in the P-BFD group and insignificantly in the other groups. Conversely, both ACTH and cortisol significantly (P &lt; 0.05) increased only in the A-BFD group, without any significant changes in both controls and P-BFD women. The analysis of the interaction between meals and groups clearly indicated that the cortisol response to the HLP-meal and the HCHO-meal was significantly different (P &lt; 0.025) between the two obese groups, the A-BFD group being characterized by a significantly lower response to the HLP-meal and a significantly higher response to the HCHO-meal, compared with the P-BFD group. Considering all groups together and after adjusting for body mass index, a highly significant relationship was found between cortisol-area under the curve and ACTH-area under the curve after each meal test. However, no relationships were found between changes in ACTH and cortisol and those of glucose, insulin, and the glucose:insulin ratio after each meal. Therefore, our data demonstrate that the response of the HPA axis to meals containing different macronutrient proportions may depend on the pattern of body fat distribution. We also suggest that the activation of the HPA axis following the ingestion of large amounts of carbohydrates may have some pathophysiological relevance, specifically in women with the abdominal obesity phenotype.


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