To date, one of the best treatments available for morbid obesity is bariatric surgery to quickly reduce body fat and the factors associated with obesity-related disease; however, the effects of vertical sleeve gastrectomy (SG) on plasma ET-1 have not been described.
This study determined the content of lipids (ceramide [CER], diacylglycerol [DAG], triacylglycerol, and free fatty acid [FFA]) and the expression of fatty acid translocase (FAT/CD36) and plasma membrane fatty acid-binding protein in visceral adipose tissue (VAT) and subcutaneous adipose tissue of women with morbid obesity without metabolic syndrome (MetSx-) or with metabolic syndrome (MetSx+) and compared the results with those of lean controls without metabolic syndrome.
Serum FGF21 was positively and significantly correlated to the expression of UCP1 (<i>r</i> = 0.56, <i>p</i> = 0.02) and TBX1 (<i>r</i> = 0.62, <i>p</i> = 0.01), however, this correlation was missing in patients with severe obesity.
We aimed to explore the relationship between GLP-1 receptor (GLP-1R) expression in adipose tissue (AT) and incretin secretion, glucose homeostasis and weight loss, in patients with morbid obesity and type 2 diabetes undergoing bariatric surgery.
Two-level repeated measures mixed models examined changes in cardiovascular health outcomes (body mass index [BMI], skinfold thickness, systolic/diastolic blood pressure percentile [SBPP/DBPP], cardiorespiratory fitness [PACER]) in youth with severe obesity over 1- and 2-year follow-up.
We found that firstly, rat insulin-2 promoter-Cre (RIP-Cre)-mediated p62 inactivation did not cause body weight gain, although ubiquitous inactivation of p62 was previously shown to result in severe obesity.
We found that firstly, rat insulin-2 promoter-Cre (RIP-Cre)-mediated p62 inactivation did not cause body weight gain, although ubiquitous inactivation of p62 was previously shown to result in severe obesity.
We found that firstly, rat insulin-2 promoter-Cre (RIP-Cre)-mediated p62 inactivation did not cause body weight gain, although ubiquitous inactivation of p62 was previously shown to result in severe obesity.
The objective of our study was to investigate the relationship between NFKB1 gene variations and the risk of MO in the context of the high/normal level of liver enzymes such as Alanine aminotransferase (ALT), Aspartate aminotransferase (AST), gamma-glutamyl transpeptidase (GGT), and alkaline phosphatase (ALP).
We found that firstly, rat insulin-2 promoter-Cre (RIP-Cre)-mediated p62 inactivation did not cause body weight gain, although ubiquitous inactivation of p62 was previously shown to result in severe obesity.
In addition, the amount of skeletal muscle perilipin 2 protein per intramyocellular lipid is reduced in subjects with morbid obesity, resulting in qualitative alterations in perilipin 2 coat around some lipid droplets.
The objective of our study was to investigate the relationship between NFKB1 gene variations and the risk of MO in the context of the high/normal level of liver enzymes such as Alanine aminotransferase (ALT), Aspartate aminotransferase (AST), gamma-glutamyl transpeptidase (GGT), and alkaline phosphatase (ALP).
(CXCR3) ligands are important regulators of angiogenesis in different disease contexts such as cancer; however, their role in human morbid obesity is unknown.
The objective of our study was to investigate the relationship between NFKB1 gene variations and the risk of MO in the context of the high/normal level of liver enzymes such as Alanine aminotransferase (ALT), Aspartate aminotransferase (AST), gamma-glutamyl transpeptidase (GGT), and alkaline phosphatase (ALP).
We found that firstly, rat insulin-2 promoter-Cre (RIP-Cre)-mediated p62 inactivation did not cause body weight gain, although ubiquitous inactivation of p62 was previously shown to result in severe obesity.
Two-level repeated measures mixed models examined changes in cardiovascular health outcomes (body mass index [BMI], skinfold thickness, systolic/diastolic blood pressure percentile [SBPP/DBPP], cardiorespiratory fitness [PACER]) in youth with severe obesity over 1- and 2-year follow-up.
University hospital, United States METHODS: Spexin, body mass index (BMI), insulin, glucose, total and high molecular weight adiponectin, leptin, and high sensitivity C- reactive protein were measured longitudinally (baseline, 6 mo, and 12 mo) after RYGB surgery in girls with severe obesity (n = 12; age = 16.7 ± 1.5 years; BMI = 51.6 ± 2.9 kg/m<sup>2</sup>).
We found that firstly, rat insulin-2 promoter-Cre (RIP-Cre)-mediated p62 inactivation did not cause body weight gain, although ubiquitous inactivation of p62 was previously shown to result in severe obesity.
We report the case of a 10 year old male with severe obesity who presented with a 2 year history of significant growth failure and excessive weight gain that was subsequently diagnosed with serum negative Hashimoto's thyroiditis and acquired hypothyroidism.