scholarly journals The Relationship Between Brown Adipose Tissue Content in Supraclavicular Fat Depots and Insulin Sensitivity in Patients with Type 2 Diabetes Mellitus and Prediabetes

2017 ◽  
Vol 19 (2) ◽  
pp. 96-102 ◽  
Author(s):  
Ekaterina Koksharova ◽  
Dmitry Ustyuzhanin ◽  
Yury Philippov ◽  
Alexander Mayorov ◽  
Marina Shestakova ◽  
...  
2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Constantin Lapa ◽  
Paula Arias-Loza ◽  
Nobuyuki Hayakawa ◽  
Hiroshi Wakabayashi ◽  
Rudolf A. Werner ◽  
...  

2020 ◽  
Vol 2 (1) ◽  
Author(s):  
Naglaa Raafat AbdRaboh ◽  
Aeman M. Asif ◽  
Sumbal Riaz ◽  
Hafez A. Ahmed

The white adipose tissue (WAT) mass in adult humans ranges between 10-35 kg. The cells are normally sensitive to insulin in the fed state, and to glucagon and adrenaline in fasting or during exercise. Well-fed sedentary individuals are prone to weight gain as they fall victims to the anabolic mechanisms led mainly by insulin. Brown adipose tissue (BAT), by contrast, stores smaller amounts of triglycerides in multi-locular droplets, is highly vascularized and its cells are rich in unique mitochondria which are capable of uncoupling oxidation from phosphorylation or ATP formation. The tissue is innerved by the sympathetic nervous system and is highly sensitive to iodothyronines. It releases heat in the body in response to sympathetic activity. BAT unique mitochondria express numerous cristae and, unlike ordinary mitochondria on other body cells including WAT cells, they express uncoupling protein-1 (UCP-1, or thermogenin). UCP-1 allows the mitochondria to oxidize more fat and glucose as they escape the controlling mechanisms that depend on the coupling of oxidation to the demand for ATP, i.e., uncouples oxidative phosphorylation. Thermogenin (UCP-1) is a natural un-coupler of oxidative phosphorylation as it dissipates the proton gradient generated across the inner mitochondrial membrane, which is required to attain a certain level for the activation of ATP synthesis in mitochondrial matrix. In BAT, ATP synthesis is inhibited, as the protons are dissipated, and most energy is released as heat. The different proportions and activity of BAT and WAT in different individuals might explain why some people are more prone to weight gain, and find it difficult to lose weight, than others; and also explains the tendency for weight gain as individuals get older. New approaches in the battle against obesity, metabolic syndrome and type 2 diabetes mellitus are expected through better understanding of how this balance between WAT and BAT is controlled. Interestingly, long term adrenergic stimulation of WAT induces browning of some white adipocytes, and the tissue gradually turns into & quot; beige & quot; adipose tissue, which shares characteristics of brown adipose tissue like thermogenesis, larger number of mitochondria and smaller lipid droplets, all developing in a gradual way. The adipose tissue interconverts its cell types in order to adapt for the changing metabolic balance and other stimuli. This phenomenon is currently incompletely understood, albeit significant for our understanding of obesity, metabolic syndrome and type 2 diabetes mellitus and many consequent complications of insulin resistance. Moreover, the nervous system is involved in the regulation of WAT and BAT through effects on fat cell proliferation, differentiation, trans-differentiation and apoptosis. The brain interacts with different adipocytes and adipokines in the pathogenesis of obesity, type 2 diabetes mellitus, anorexia, cachexia and other syndromes. This review will target many of these aspects in an attempt to draw more attention in the direction of this major health issue.


Author(s):  
Ismail Baloglu ◽  
Kultigin Turkmen ◽  
Nedim Selcuk ◽  
Halil Tonbul ◽  
Adalet Ozcicek ◽  
...  

Abstract Introduction and aim Cardiovascular diseases remain the most common cause of morbidity and mortality in patients with diabetes. Epicardial adipose tissue (EAT), visceral fat depot of the heart, was found to be associated with coronary artery disease in cardiac and non-cardiac patients. Increased visceral adiposity is associated with proinflammatory activity, impaired insulin sensitivity, increased risk of atherosclerosis and high mortality. In the present study we aimed to investigate the relationship between EAT and visceral adiposity index (VAI) in patients with diabetes. Methods This was a cross-sectional study involving 128 patients with type 2 diabetes mellitus (73 females, 55 males; mean age, 54.09+±+9.17 years) and 32 control subjects (23 females, 9 males; mean age, 50.09+±+7.81 years). EAT was measured by using a trans-thoracic echocardiograph. Parameters such as waist circumference (WC), body mass index (BMI), triglyceride and high density lipoprotein (HDL) cholesterol were used to calculate VAI. Result EAT and VAI measurements were significantly higher in patients with diabetes when compared to control subjects. In the bivariate correlation analysis, VAI was positively correlated with uric acid level (r=0.214, p=0.015), white blood cell count (r= 0.262, p=0.003), platelet count (r=0.223, p=0.011) and total cholesterol levels (r= 0.363, p<0.001). Also, VAI was found to be the independent predictor of EAT. Conclusion Simple calculation of VAI was found to be associated with increased EAT in patients with type 2 diabetes.


2018 ◽  
Vol 127 (08) ◽  
pp. 550-556 ◽  
Author(s):  
Melina Amor ◽  
Bianca K. Itariu ◽  
Veronica Moreno-Viedma ◽  
Magdalena Keindl ◽  
Alexander Jürets ◽  
...  

AbstractObesity and type 2 diabetes mellitus have reached an epidemic level, thus novel treatment concepts need to be identified. Myostatin, a myokine known for restraining skeletal muscle growth, has been associated with the development of insulin resistance and type 2 diabetes mellitus. Yet, little is known about the regulation of myostatin in human obesity and insulin resistance. We aimed to investigate the regulation of myostatin in obesity and uncover potential associations between myostatin, metabolic markers and insulin resistance/sensitivity indices. Circulating active myostatin concentration was measured in the serum of twenty-eight severely obese non-diabetic patients compared to a sex and age matched lean and overweight control group (n=22). Insulin resistance/sensitivity was assessed in the obese group. Skeletal muscle and adipose tissue specimens from the obese group were collected during elective bariatric surgery. Adipose tissue samples from lean and overweight subjects were collected during elective abdominal surgery. Myostatin concentration was increased in obese compared to lean individuals, while myostatin adipose tissue expression did not differ. Muscle myostatin gene expression strongly correlated with expression of metabolic genes such as IRS1, PGC1α, SREBF1. Circulating myostatin concentration correlated positively with insulin resistance indices and negatively with insulin sensitivity indices. The best correlation was obtained for the oral glucose insulin sensitivity index. Our results point to an interesting correlation between myostatin and insulin resistance/sensitivity in humans, and emphasize its need for further evaluation as a pharmacological target in the prevention and treatment of obesity-associated metabolic complications.


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