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Ο σύνδεσμος αποθηκεύεται στο πρόχειρο
Σελίδα 1 από 27 Αποτελέσματα
Excess visceral adipose tissue/ectopic fat the missing link in the obesity paradox?
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Characterization of Ageing- and Diet-Related Swine Models of Sarcopenia and Sarcopenic Obesity.
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Σύνδεση εγγραφή
Sarcopenia and sarcopenic obesity are currently considered major global threats for health and well-being. However, there is a lack of adequate preclinical models for their study. The present trial evaluated the suitability of aged swine by determining changes in adiposity, fatty acids composition,
Ectopic UCP1 Overexpression in White Adipose Tissue Improves Insulin Sensitivity in Lou/C Rats, a Model of Obesity Resistance.
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Brown adipose tissue (BAT), characterized by the presence of uncoupling protein 1 (UCP1), has been described as metabolically active in humans. Lou/C rats, originating from the Wistar strain, are resistant to obesity. We previously demonstrated that Lou/C animals express UCP1 in beige adipocytes in
Mitochondrial proton leak in obesity-resistant and obesity-prone mice.
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We quantified uncoupling proteins (UCPs) in molar amounts and assessed proton conductance in mitochondria isolated from interscapular brown adipose tissue (IBAT) and hindlimb muscle [known from prior work to contain ectopic brown adipose tissue (BAT) interspersed between muscle fibers] of
Adipose Tissue Dysfunction as Determinant of Obesity-Associated Metabolic Complications.
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Obesity is a critical risk factor for the development of type 2 diabetes (T2D), and its prevalence is rising worldwide. White adipose tissue (WAT) has a crucial role in regulating systemic energy homeostasis. Adipose tissue expands by a combination of an increase in adipocyte size (hypertrophy) and
The distinction of metabolically 'healthy' from 'unhealthy' obese individuals.
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OBJECTIVE
The prevalence and severity of obesity are dramatically increasing throughout the world. Obesity causes a decline in life expectancy due to its associated metabolic and cardiovascular comorbid disorders. Therefore, it will become more important to distinguish obese individuals at high risk
Altered DNA methylation in liver and adipose tissues derived from individuals with obesity and type 2 diabetes.
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Obesity is a well-recognized risk factor for insulin resistance and type 2 diabetes (T2D), although the precise mechanisms underlying the relationship remain unknown. In this study we identified alterations of DNA methylation influencing T2D pathogenesis, in subcutaneous and visceral adipose
Obesity Phenotypes, Diabetes, and Cardiovascular Diseases
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This review addresses the interplay between obesity, type 2 diabetes mellitus, and cardiovascular diseases. It is proposed that obesity, generally defined by an excess of body fat causing prejudice to health, can no longer be evaluated solely by the body mass index (expressed in kg/m2)
Role of obesity and lipotoxicity in the development of nonalcoholic steatohepatitis: pathophysiology and clinical implications.
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As obesity reaches epidemic proportions, nonalcoholic fatty liver disease (NAFLD) is becoming a frequent cause of patient referral to gastroenterologists. There is a close link between dysfunctional adipose tissue in NAFLD and common conditions such as metabolic syndrome, type 2 diabetes mellitus,
Implications of 2H-labeling of DNA protocol to measure in vivo cell turnover in adipose tissue.
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Adipose tissue expansion in obesity involves a series of cycles of adipocyte hyperplasia, hypertrophy and hypoplasia due to alterations in adipogenesis, adipocyte cellular metabolism and cell death, respectively. Increased frequency of these cycles may lead to deterioration of adipocyte function and
Chemical imaging of lipid droplets in muscle tissues using hyperspectral coherent Raman microscopy.
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The accumulation of lipids in non-adipose tissues is attracting increasing attention due to its correlation with obesity. In muscle tissue, ectopic deposition of specific lipids is further correlated with pathogenic development of insulin resistance and type 2 diabetes. Most intramyocellular lipids
Impact of different fat depots on insulin sensitivity: predominant role of liver fat.
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BACKGROUND
Overall obesity and, as it is increasingly appreciated, body fat distribution and ectopic fat deposition in liver and skeletal muscle, determine insulin resistance in humans. However, little is known about the independence of these relationships. Therefore, we determined the impact of
Optimal diet and lifestyle strategies for the management of cardio-metabolic risk.
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Cardio-metabolic risk (CMR) embodies a clustering of metabolic abnormalities that increase the likelihood of developing CVD in the large arteries of the heart, peripheral tissues and brain. These abnormalities share a common origin of insulin resistance, which manifests typically as excess visceral
Loss of FTO antagonises Wnt signaling and leads to developmental defects associated with ciliopathies.
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Common intronic variants in the Human fat mass and obesity-associated gene (FTO) are found to be associated with an increased risk of obesity. Overexpression of FTO correlates with increased food intake and obesity, whilst loss-of-function results in lethality and severe developmental defects.
Structural analysis of protein tyrosine phosphatase 1B reveals potentially druggable allosteric binding sites.
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Catalytic proteins such as human protein tyrosine phosphatase 1B (PTP1B), with conserved and highly polar active sites, warrant the discovery of druggable nonactive sites, such as allosteric sites, and potentially, therapeutic small molecules that can bind to these sites. Catalyzing the
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