Strength training improves insulin sensitivity and plasma lipid levels without altering body composition in overweight and obese subjects

2011 ◽  
Vol 58 (4) ◽  
pp. 169-174 ◽  
Author(s):  
Óscar Hernán Jiménez ◽  
Robinson Ramírez-Vélez
2009 ◽  
Vol 161 (6) ◽  
pp. 845-852 ◽  
Author(s):  
Labros Melistas ◽  
Christos S Mantzoros ◽  
Meropi Kontogianni ◽  
Smaragdi Antonopoulou ◽  
Jose M Ordovas ◽  
...  

ObjectiveWe explored potential associations of two single nucleotide polymorphisms (SNPs) in the adiponectin gene (ADIPOQ; +45T>G, rs2241766 and +276G>T, rs1501299) with circulating total and high-molecular weight (HMW) adiponectin, insulin resistance (IR), and markers of obesity in a healthy Greek female population.Design and methodsThe two SNPs were genotyped in 349 women without diabetes (mean age: 47.0±12.1 years, mean body mass index: 28.9±5.6 kg/m2). Total and HMW adiponectin concentrations, body composition variables, IR parameters, and plasma lipid levels were determined.ResultsIn single SNP analysis adjusting for several potential confounders, SNP +276G>T was associated with higher fasting insulin levels (P=0.01) and higher homeostasis model assessment index for IR (HOMA-IR; P=0.009), and SNP +45T>G was associated with lower insulin levels and HOMA-IR (P=0.05 and P=0.07 respectively). No association with total or HMW adiponectin, plasma lipid levels, and body composition variables was observed; however, haplotype analysis revealed that subjects homozygous for the most common +45T/+276G haplotype had lower total adiponectin levels than did noncarriers of this haplotype (P=0.02). The observed differences in HOMA-IR were very significant among women with a higher body fat (BF) percentage (≥ the population median of 41%; all P≤0.005), but not among leaner individuals (P for interactions 0.01–0.07), thus suggesting that ADIPOQ effects on insulin sensitivity may depend upon BF status.ConclusionOur data suggest a significant role of ADIPOQ variants at positions +45 and +276 in the development of IR in healthy Greek women possibly through an interaction with BF.


2004 ◽  
Vol 36 (Supplement) ◽  
pp. S243
Author(s):  
Paul J. Arciero ◽  
Roger M. Pressman ◽  
Bradley C. Nindl ◽  
Matthew D. Vukovich ◽  
Michael J. Ormsbee ◽  
...  

2016 ◽  
Vol 122 (4) ◽  
pp. 167-179 ◽  
Author(s):  
Torgrim Mikal Langleite ◽  
Jørgen Jensen ◽  
Frode Norheim ◽  
Hanne Løvdal Gulseth ◽  
Daniel Steensen Tangen ◽  
...  

2017 ◽  
Vol 8 (4) ◽  
pp. 557-562 ◽  
Author(s):  
J. Most ◽  
G.H. Goossens ◽  
D. Reijnders ◽  
E.E. Canfora ◽  
J. Penders ◽  
...  

Gut microbiota composition may play an important role in the development of obesity-related comorbidities. However, only few studies have investigated gender-differences in microbiota composition and gender-specific associations between microbiota or microbial products and insulin sensitivity. Insulin sensitivity (hyperinsulinemic-euglycemic clamp), body composition (dual energy X-ray absorptiometry), substrate oxidation (indirect calorimetry), systemic inflammatory markers and microbiota composition (PCR) were determined in male (n=15) and female (n=14) overweight and obese subjects. Bacteroidetes/Firmicutes-ratio was higher in men than in women (P=0.001). Bacteroidetes/Firmicutes-ratio was inversely related to peripheral insulin sensitivity only in men (men: P=0.003, women: P=0.882). This association between Bacteroidetes/Firmicutes-ratio and peripheral insulin sensitivity did not change after adjustment for dietary fibre and saturated fat intake, body composition, fat oxidation and markers of inflammation. Bacteroidetes/Firmicutes-ratio was not associated with hepatic insulin sensitivity. Men and women differ in microbiota composition and its impact on insulin sensitivity, implying that women might be less sensitive to gut microbiota-induced metabolic aberrations than men. This trial was registered at clinicaltrials.gov as NCT02381145.


2003 ◽  
Vol 112 (5-6) ◽  
pp. 610-616 ◽  
Author(s):  
Coleen M. Damcott ◽  
Eleanor Feingold ◽  
Susan P. Moffett ◽  
M. Michael Barmada ◽  
Julie A. Marshall ◽  
...  

2006 ◽  
Vol 91 (12) ◽  
pp. 5107-5112 ◽  
Author(s):  
E. Klimcakova ◽  
J. Polak ◽  
C. Moro ◽  
J. Hejnova ◽  
M. Majercik ◽  
...  

Abstract Context: Obesity is characterized by a low-grade inflammatory state, which could play a role in insulin resistance. Dynamic strength training improves insulin sensitivity. Objective: The objective of this study was to investigate, in obese subjects, whether the insulin sensitizing effect of dynamic strength training is associated with changes in plasma levels and gene expression of adipokines potentially involved in the development of insulin resistance. Design: Twelve obese male subjects were investigated before and at the end of 3 months of dynamic strength training. Insulin sensitivity was evaluated using euglycemic-hyperinsulinemic clamp. Blood samples and needle biopsy samples of sc abdominal adipose tissue were obtained. The plasma levels and adipose tissue mRNA levels of adiponectin, leptin, IL-1β, IL-6, and TNF-α were determined. Results: The training induced an increase in the whole-body glucose disposal rate by 24% (P = 0.04). The body weight was not altered during the training. Plasma levels of leptin decreased during the training (16.6 ± 6.3 vs. 13.1 ± 5.7 ng/ml) by 21% (P < 0.02), whereas no change in plasma levels of other adipokines and C-reactive protein was observed. Gene expression of the investigated adipokines was not changed in sc adipose tissue during the training. Conclusions: In obese subjects, the dynamic strength training resulted in an improvement of whole-body insulin sensitivity. The increase in insulin sensitivity was not associated with training-induced modifications of plasma levels or adipose tissue gene expression of adipokines supposedly involved in the development of insulin resistance.


Sign in / Sign up

Export Citation Format

Share Document