SGAs Increase Teens’ Abdominal Fat, Decrease Insulin Sensitivity

2018 ◽  
Vol 53 (16) ◽  
Author(s):  
Mark Moran
2015 ◽  
Vol 7 (S1) ◽  
Author(s):  
Anize Delfino von Frankenberg ◽  
Anna Marina ◽  
Xiaoling Song ◽  
Holly S Callahan ◽  
Mario Kratz ◽  
...  

2009 ◽  
Vol 296 (2) ◽  
pp. E351-E357 ◽  
Author(s):  
Jonathan Q. Purnell ◽  
Steven E. Kahn ◽  
Mary H. Samuels ◽  
David Brandon ◽  
D. Lynn Loriaux ◽  
...  

Controversy exists as to whether endogenous cortisol production is associated with visceral obesity and insulin resistance in humans. We therefore quantified cortisol production and clearance rates, abdominal fat depots, insulin sensitivity, and adipocyte gene expression in a cohort of 24 men. To test whether the relationships found are a consequence rather than a cause of obesity, eight men from this larger group were studied before and after weight loss. Daily cortisol production rates (CPR), free cortisol levels (FC), and metabolic clearance rates (MCR) were measured by stable isotope methodology and 24-h sampling; intra-abdominal fat (IAF) and subcutaneous fat (SQF) by computed tomography; insulin sensitivity (SI) by frequently sampled intravenous glucose tolerance test; and adipocyte 11β-hydroxysteroid dehydrogenase-1 (11β-HSD-1) gene expression by quantitative RT-PCR from subcutaneous biopsies. Increased CPR and FC correlated with increased IAF, but not SQF, and with decreased SI. Increased 11β-HSD-1 gene expression correlated with both IAF and SQF and with decreased SI. With weight loss, CPR, FC, and MCR did not change compared with baseline; however, with greater loss in body fat than lean mass during weight loss, both CPR and FC increased proportionally to final fat mass and IAF and 11β-HSD-1 decreased compared with baseline. These data support a model in which increased hypothalamic-pituitary-adrenal activity in men promotes selective visceral fat accumulation and insulin resistance and may promote weight regain after diet-induced weight loss, whereas 11β-HSD-1 gene expression in SQF is a consequence rather than cause of adiposity.


Obesity ◽  
2009 ◽  
Vol 17 (1) ◽  
pp. 188-195 ◽  
Author(s):  
Soo Lim ◽  
Kyu R. Son ◽  
In C. Song ◽  
Ho S. Park ◽  
Cheng J. Jin ◽  
...  

2000 ◽  
Vol 50 ◽  
pp. 61 ◽  
Author(s):  
Yoshinori Miyazaki ◽  
Archana Mahankali ◽  
Masafumi Matsuda ◽  
Srikanth Mahankali ◽  
Kenneth Cusi ◽  
...  

2005 ◽  
Vol 288 (4) ◽  
pp. E768-E774 ◽  
Author(s):  
Kirsi Hannele Pietiläinen ◽  
Aila Rissanen ◽  
Jaakko Kaprio ◽  
Sari Mäkimattila ◽  
Anna-Maija Häkkinen ◽  
...  

We determined whether acquired obesity is associated with increases in liver or intra-abdominal fat or impaired insulin sensitivity by studying monozygotic (MZ) twin pairs discordant and concordant for obesity. We studied nineteen 24- to 27-yr-old MZ twin pairs, with intrapair differences in body weight ranging from 0.1 to 24.7 kg [body mass index (BMI) range 20.0–33.9 kg/m2], identified from a population-based FinnTwin16 sample. Fat distribution was determined by magnetic resonance imaging, percent body fat by dual-energy X-ray absorptiometry, liver fat by proton spectroscopy, insulin sensitivity by measuring the fasting insulin concentration, and whole body insulin sensitivity by the euglycemic insulin clamp technique. Intrapair differences in BMI were significantly correlated with those in intra-abdominal fat ( r = 0.82, P < 0.001) and liver fat ( r = 0.57, P = 0.010). Intrapair differences in fasting insulin correlated with those in subcutaneous abdominal ( r = 0.60, P = 0.008), intra-abdominal ( r = 0.75, P = 0.0001) and liver ( r = 0.49, P = 0.048) fat. Intrapair differences in whole body insulin sensitivity correlated with those in subcutaneous abdominal ( r = −0.72, P = 0.001) and intra-abdominal ( r = −0.55, P = 0.015) but not liver ( r = −0.20, P = 0.20) fat. We conclude that acquired obesity is associated with increases in intra-abdominal and liver fat and insulin resistance, independent of genetic factors.


2021 ◽  
Vol 12 ◽  
Author(s):  
Kristoffer Jensen Kolnes ◽  
Maria Houborg Petersen ◽  
Teodor Lien-Iversen ◽  
Kurt Højlund ◽  
Jørgen Jensen

In obesity, excessive abdominal fat, especially the accumulation of visceral adipose tissue (VAT), increases the risk of metabolic disorders, such as type 2 diabetes mellitus (T2DM), cardiovascular disease, and non-alcoholic fatty liver disease. Excessive abdominal fat is associated with adipose tissue dysfunction, leading to systemic low-grade inflammation, fat overflow, ectopic lipid deposition, and reduced insulin sensitivity. Physical activity is recommended for primary prevention and treatment of obesity, T2DM, and related disorders. Achieving a stable reduction in body weight with exercise training alone has not shown promising effects on a population level. Because fat has a high energy content, a large amount of exercise training is required to achieve weight loss. However, even when there is no weight loss, exercise training is an effective method of improving body composition (increased muscle mass and reduced fat) as well as increasing insulin sensitivity and cardiorespiratory fitness. Compared with traditional low-to-moderate-intensity continuous endurance training, high-intensity interval training (HIIT) and sprint interval training (SIT) are more time-efficient as exercise regimens and produce comparable results in reducing total fat mass, as well as improving cardiorespiratory fitness and insulin sensitivity. During high-intensity exercise, carbohydrates are the main source of energy, whereas, with low-intensity exercise, fat becomes the predominant energy source. These observations imply that HIIT and SIT can reduce fat mass during bouts of exercise despite being associated with lower levels of fat oxidation. In this review, we explore the effects of different types of exercise training on energy expenditure and substrate oxidation during physical activity, and discuss the potential effects of exercise training on adipose tissue function and body fat distribution.


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