Relative contribution of muscle and liver insulin resistance to dysglycemia in postmenopausal overweight and obese women: A MONET group study

2017 ◽  
Vol 78 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Belinda Elisha ◽  
Emmanuel Disse ◽  
Katherine Chabot ◽  
Nadine Taleb ◽  
Denis Prud’homme ◽  
...  
Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 2048-P
Author(s):  
BENJAMIN J. RYAN ◽  
DOUGLAS W. VAN PELT ◽  
LISA M. GUTH ◽  
ALISON LUDZKI ◽  
RACHEL A. GIOSCIA-RYAN ◽  
...  

2014 ◽  
Vol 10 (2) ◽  
pp. 111-118 ◽  
Author(s):  
Nourhen Mezghanni ◽  
Mouna Mnif ◽  
Hamdi Chtourou ◽  
Khansa Chaabouni ◽  
Liwa Masmoudi ◽  
...  

2017 ◽  
Vol 13 (10) ◽  
pp. S104-S105
Author(s):  
Carolina F Nicoletti ◽  
Vitor Pinhanelli ◽  
Marcela Pinhel ◽  
Natalia Noronha ◽  
Bruno de Oliveira ◽  
...  

2010 ◽  
Vol 2010 ◽  
pp. 1-8 ◽  
Author(s):  
Fernando Cordido ◽  
Jesús Garcia-Buela ◽  
Susana Sangiao-Alvarellos ◽  
Teresa Martinez ◽  
Ovidio Vidal

The aim of the present study was to evaluate the relationship between GHRH-induced GH secretion in obese premenopausal women and cardiovascular risk markers or insulin resistance. Premenopausal obese women, aged 35–52 years, were studied. GH secretion, IGF-I, serum cardiovascular risk markers, insulin, leptin, mid-waist and hip circumference, total body fat, and truncal fat were measured. Subjects were classified as meeting the criteria for GH deficiency (GHD) when peak GH after stimulation with GHRH was≤3 μg/L. Mean total and LDL cholesterol, fasting insulin, and HOMA-IR were all higher, in subjects who would have been classified as GH-deficient compared with GH-sufficient. Peak GH secretion after stimulation was inversely associated with fasting insulin (R=−0.650,P=.012), HOMA-IR (R=−0.846,P=.001), total cholesterol (R=−0.532,P=.034), and LDL cholesterol (R=−0.692,P=.006) and positively associated with HDL cholesterol (R=0.561,P=.037). These data strongly suggest a role for insulin resistance in the decreased GH secretion of obesity and that the blunted GH secretion of central obesity could be the pituitary expression of the metabolic syndrome.


2019 ◽  
Vol 241 (3) ◽  
pp. 293-305 ◽  
Author(s):  
Srilaxmi Kalavalapalli ◽  
Fernando Bril ◽  
Joy Guingab ◽  
Ariana Vergara ◽  
Timothy J Garrett ◽  
...  

Exenatide (Exe) is a glucagon-like peptide (GLP)-1 receptor agonist that enhances insulin secretion and is associated with induction of satiety with weight loss. As mitochondrial dysfunction and lipotoxicity are central features of nonalcoholic steatohepatitis (NASH), we tested whether Exe improved mitochondrial function in this setting. We studied C57BL/6J mice fed for 24 weeks either a control- or high-fructose, high-trans-fat (TFD)-diet (i.e., a NASH model previously validated by our laboratory). For the final 8 weeks, mice were treated with Exe (30 µg/kg/day) or vehicle. Mitochondrial metabolism was assessed by infusion of [13C3]propionate, [3,4-13C2]glucose and NMR-based 13C-isotopomer analysis. Exenatide significantly decreased fasting plasma glucose, free fatty acids and triglycerides, as well as adipose tissue insulin resistance. Moreover, Exe reduced 23% hepatic glucose production, 15% tri-carboxylic acid (TCA) cycle flux, 20% anaplerosis and 17% pyruvate cycling resulting in a significant 31% decrease in intrahepatic triglyceride content (P = 0.02). Exenatide improved the lipidomic profile and decreased hepatic lipid byproducts associated with insulin resistance and lipotoxicity, such as diacylglycerols (TFD: 111 ± 13 vs Exe: 64 ± 13 µmol/g protein, P = 0.03) and ceramides (TFD: 1.6 ± 0.1 vs Exe: 1.3 ± 0.1 µmol/g protein, P = 0.03). Exenatide lowered expression of hepatic lipogenic genes (Srebp1C, Cd36) and genes involved in inflammation and fibrosis (Tnfa, Timp1). In conclusion, in a diet-induced mouse model of NASH, Exe ameliorates mitochondrial TCA cycle flux and significantly decreases insulin resistance, steatosis and hepatocyte lipotoxicity. This may have significant clinical implications to the potential mechanism of action of GLP-1 receptor agonists in patients with NASH. Future studies should elucidate the relative contribution of direct vs indirect mechanisms at play.


Author(s):  
Moushira Zaki ◽  
Sanaa Kamal ◽  
Mona Abd Elmotaleb A. Hussein ◽  
Hend M. Tawfeek ◽  
Mina Wassef Girgiss ◽  
...  

Background: Chemerin has been newly defined to be released from mature adipocytes and the chemerin concentrations in human serum augmented with obesity. There is a subclinical chronic low-grade inflammatory response where insulin resistance (IR) may develop. The aim of this study is to expound the prospective role of chemerin the in inflammation. Also, investigate relation between chemerin and serum lipid, glucose, body fat percentage, and metabolic parameters in obese and lean women with IR. Lymphocytes and neutrophils play a major role in inflammation and comprise the first line of defense against infection. The ratio of absolute neutrophil count to lymphocyte count, the neutrophil-to-lymphocyte ratio (NLR), determined as is a novel inflammatory biomarker utilized as a prognostic factor in numerous diseases Methods: This study was designed to investigate serum chemerin, NLR, and high-sensitive C-reactive protein (hsCRP) levels in 50 obese women with IR and 50 lean healthy women. Results: Obese group had significant higher levels of serum chemerin, NLR, hsCRP levels and metabolic parameters than lean one. Chemerin also correlated positively with NLR inflammatory marker and body mass index (BMI). Neutrophil‐to‐lymphocyte ratio was related to pro‐inflammatory Conclusion: The present study elucidates that chemerin levels are concomitant with obesity and IR and could play a role in the inflammation, having key aspects of metabolic syndrome.


2013 ◽  
Vol 7 (5) ◽  
pp. 723-730 ◽  
Author(s):  
Aneta Mankowska-Cyl ◽  
Magdalena Krintus ◽  
Pawel Rajewski ◽  
Grazyna Sypniewska

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