Insulin Sensitivity Measured With the Minimal Model is Higher in Moderately Overweight Women With Predominantly Lower Body Fat

1999 ◽  
Vol 31 (07) ◽  
pp. 415-417 ◽  
Author(s):  
E. Raynaud ◽  
A. Pérez-Martin ◽  
J. Brun ◽  
C. Fédou ◽  
J. Mercier
Circulation ◽  
2018 ◽  
Vol 137 (suppl_1) ◽  
Author(s):  
Katherine H Ingram ◽  
Roxanna Lopez

An association between abdominal adiposity and insulin resistance is well-established. Recent research indicates that subcutaneous fat accumulation in the lower body may be associated with higher levels of insulin sensitivity. Hypothesis: This pilot study tested the hypothesis that the distribution of body fat in the lower body after pregnancy is negatively associated with gestational insulin resistance. Methods: In 32 nulliparous pregnant women (age 27±4.5, BMI 29.5±7.9, 69% non-hispanic white), the Homeostasis Model Assessment of Insulin Resistance (HOMA-IR) was computed from fasting glucose and insulin at 24-28 weeks gestation. Body composition was assessed at mid-gestation (18-20 weeks) and at four weeks post-partum. Total body fat was estimated via bioelectrical impedance (InBody 720) and skinfold thicknesses were measured at seven sites. Dual-energy xray absorptiometry (DXA) measures of regional fat (gynoid, visceral, and leg) were obtained post-partum only. Gestational weight gain was monitored by medical records. Partial correlation analyses were controlled for age and race and then analyses were repeated controlling for baseline (mid-gestation) body fat percent. HOMA-IR was log-transformed for normality. Results: HOMA-IR was associated with post-partum body fat ( r =0.45, p < .05) and adiposity in the trunk region ( r =0.58, 0.57 and 0.52 for DXA visceral fat, suprailiac skinfold, and abdominal skinfold, respectively, p < .01), but not with gestational weight gain ( r =.07, p = ns), DXA gynoid region ( r = 0.26, p = ns), or any other leg measure. When analyses were further controlled for baseline body fat, post-partum measures of lower-body adiposity were strongly and negatively correlated with HOMA-IR ( r = -0.66, -0.48, and -0.48 for thigh skinfold, DXA gynoid, and DXA leg, respectively, p < .05 for all). Neither DXA visceral fat ( r = .23; p = ns) nor any other post-partum fat measures were associated with HOMA-IR when controlling for baseline body fat. Conclusions: Gestational insulin resistance was negatively associated with post-partum thigh fat accumulation, independent of overall body fat. These data indicate that insulin sensitivity may be associated with the ability to store fat in the lower body and should warrant further study of subcutaneous leg fat as a metabolically “healthy” storage depot.


2006 ◽  
Vol 91 (5) ◽  
pp. 1698-1704 ◽  
Author(s):  
B. Buemann ◽  
A. Astrup ◽  
O. Pedersen ◽  
E. Black ◽  
C. Holst ◽  
...  

2013 ◽  
Vol 110 (8) ◽  
pp. 1534-1547 ◽  
Author(s):  
Michelle Harvie ◽  
Claire Wright ◽  
Mary Pegington ◽  
Debbie McMullan ◽  
Ellen Mitchell ◽  
...  

Intermittent energy restriction may result in greater improvements in insulin sensitivity and weight control than daily energy restriction (DER). We tested two intermittent energy and carbohydrate restriction (IECR) regimens, including one which allowedad libitumprotein and fat (IECR+PF). Overweight women (n115) aged 20 and 69 years with a family history of breast cancer were randomised to an overall 25 % energy restriction, either as an IECR (2500–2717 kJ/d, < 40 g carbohydrate/d for 2 d/week) or a 25 % DER (approximately 6000 kJ/d for 7 d/week) or an IECR+PF for a 3-month weight-loss period and 1 month of weight maintenance (IECR or IECR+PF for 1 d/week). Insulin resistance reduced with the IECR diets (mean − 0·34 (95 % CI − 0·66, − 0·02) units) and the IECR+PF diet (mean − 0·38 (95 % CI − 0·75, − 0·01) units). Reductions with the IECR diets were significantly greater compared with the DER diet (mean 0·2 (95 % CI − 0·19, 0·66) μU/unit,P= 0·02). Both IECR groups had greater reductions in body fat compared with the DER group (IECR: mean − 3·7 (95 % CI − 2·5, − 4·9) kg,P= 0·007; IECR+PF: mean − 3·7 (95 % CI − 2·8, − 4·7) kg,P= 0·019; DER: mean − 2·0 (95 % CI − 1·0, 3·0) kg). During the weight maintenance phase, 1 d of IECR or IECR+PF per week maintained the reductions in insulin resistance and weight. In the short term, IECR is superior to DER with respect to improved insulin sensitivity and body fat reduction. Longer-term studies into the safety and effectiveness of IECR diets are warranted.


2005 ◽  
Vol 29 (6) ◽  
pp. 624-631 ◽  
Author(s):  
B Buemann ◽  
T I A Sørensen ◽  
O Pedersen ◽  
E Black ◽  
C Holst ◽  
...  

Diabetes ◽  
1993 ◽  
Vol 42 (11) ◽  
pp. 1635-1641 ◽  
Author(s):  
P. A. Coates ◽  
R. L. Ollerton ◽  
S. D. Luzio ◽  
I. S. Ismail ◽  
D. R. Owens

2019 ◽  
Vol 31 (3) ◽  
pp. 212-218

Both insulin and leptin are major contributors for the body energy balance. Obesity is a state of energy imbalance and is also associated with changes in both insulin sensitivity and leptin sensitivity. The aim of this study was to find out the relationship between insulin sensitivity and body fat composition, and leptin sensitivity in non-obese and obese adults. A total of 86 adults participated: 42 non-obese and 44 over-weight/obese. Body fat (BF) percent was determined by skinfold method. Fasting plasma glucose was analyzed by glucose oxidase-phenol and 4 aminophenazone (GOD-PAP) method using spectro-photometer, fasting serum insulin and leptin concentrations by direct sandwich ELISA method and resting energy expenditure (REE) by indirect calorimetry. Leptin sensitivity index and insulin sensitivity were expressed as REE : Leptin ratio and homeostatic model assessment-insulin resistance (HOMA-IR), respectively. It was found that median value of HOMA-IR was significantly higher [2.93 vs 1.72, p<0.01] and leptin sensitivity was significantly lower [116.76 vs 265.66, p<0.001] in the overweight/obese adults than the non-obese adults, indicating that insulin sensitivity and leptin sensitivity were markedly reduced in overweight/obese adults in compare to non-obese adults. There was a moderate degree of positive relationship between HOMA-IR and BF only in the overweight/obese (ρ=0.509, n=44, p<0.001) and all adults (ρ=0.39, n=86, p<0.001). Similarly, a weak negative relationship between leptin sensitivity index and HOMA-IR was found in the overweight/obese (ρ=-0.328, n=44, p<0.05) and all adults (ρ=-0.35, n=86, p<0.01). It can be concluded that the insulin sensitivity was adiposity dependent, but, it did not depend on leptin sensitivity.


Author(s):  
Mahasampath Gowri S ◽  
Belavendra Antonisamy ◽  
Finney S. Geethanjali ◽  
Nihal Thomas ◽  
Felix Jebasingh ◽  
...  

1998 ◽  
Vol 83 (6) ◽  
pp. 1911-1915 ◽  
Author(s):  
Ramin Alemzadeh ◽  
Gina Langley ◽  
Lori Upchurch ◽  
Pam Smith ◽  
Alfred E. Slonim

Hyperinsulinemia, insulin resistance, and increased adipose tissue are hallmarks of the obesity state in both humans and experimental animals. The role of hyperinsulinemia as a possible preceding event in the development of obesity has been proposed. We previously demonstrated that administration of diazoxide (DZ), an inhibitor of insulin secretion, to obese hyperinsulinemic Zucker rats resulted in less weight gain, enhanced insulin sensitivity, and improved glucose tolerance. Assuming that hyperinsulinemia plays a major role in the development of human obesity, then its reversal should have therapeutic potential. To test this hypothesis, we conducted a randomized placebo-controlled trial in 24 hyperinsulinemic adults [body mass index (BMI) &gt; 30 kg/m2]. All subjects were placed on a low-calorie (1260 for females and 1570 for males) Optifast (Sandoz, Minneapolis, MN) diet. After an initial 1-week lead-in period, 12 subjects (mean ± se for age and BMI, 31 ± 1 and 40 ± 2, respectively) received DZ (2 mg/kg BW·day; maximum, 200 mg/day, divided into 3 doses) for 8 weeks; and 12 subjects (mean± se for age and BMI, 28 ± 1 and 43 ± 1, respectively) received placebo. Compared with the placebo group, DZ subjects had greater weight loss (9.5 ± 0.69% vs. 4.6 ± 0.61%, P &lt; 0.001), greater decrease in body fat (P &lt; 0.01), greater increase in fat-free mass to body fat ratio (P &lt; 0.01), and greater attenuation of acute insulin response to glucose (P &lt; 0.01). However, there was no significant difference in insulin sensitivity and glucose effectiveness, as determined by the insulin-modified iv glucose tolerance test (Bergman’s minimal model) and no significant difference in glycohemoglobin values. Conclusion: 8 weeks treatment with DZ had a significant antiobesity effect in hyperinsulinemic obese adults without inducing hyperglycemia.


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