scholarly journals Polymorphisms in the gene encoding adiponectin receptor 1 are associated with insulin resistance and high liver fat

Diabetologia ◽  
2005 ◽  
Vol 48 (11) ◽  
pp. 2282-2291 ◽  
Author(s):  
N. Stefan ◽  
F. Machicao ◽  
H. Staiger ◽  
J. Machann ◽  
F. Schick ◽  
...  
2006 ◽  
Vol 291 (2) ◽  
pp. E282-E290 ◽  
Author(s):  
Riikka Lautamäki ◽  
Ronald Borra ◽  
Patricia Iozzo ◽  
Markku Komu ◽  
Terho Lehtimäki ◽  
...  

Nonalcoholic fatty liver (NAFL) is a common comorbidity in patients with type 2 diabetes and links to the risk of coronary syndromes. The aim was to determine the manifestations of metabolic syndrome in different organs in patients with liver steatosis. We studied 55 type 2 diabetic patients with coronary artery disease using positron emission tomography. Myocardial perfusion was measured with [15O]H2O and myocardial and skeletal muscle glucose uptake with 2-deoxy-2-[18F]fluoro-d-glucose during hyperinsulinemic euglycemia. Liver fat content was determined by magnetic resonance proton spectroscopy. Patients were divided on the basis of their median (8%) into two groups with low (4.6 ± 2.0%) and high (17.4 ± 8.0%) liver fat content. The groups were well matched for age, BMI, and fasting plasma glucose. In addition to insulin resistance at the whole body level ( P = 0.012) and muscle ( P = 0.002), the high liver fat group had lower insulin-stimulated myocardial glucose uptake ( P = 0.040) and glucose extraction rate ( P = 0.0006) compared with the low liver fat group. In multiple regression analysis, liver fat content was the most significant explanatory variable for myocardial insulin resistance. In addition, the high liver fat group had increased concentrations of high sensitivity C-reactive protein, soluble forms of E-selectin, vascular adhesion protein-1, and intercellular adhesion molecule-1 ( P < 0.05) and lower coronary flow reserve ( P = 0.02) compared with the low liver fat group. In conclusion, in patients with type 2 diabetes and coronary artery disease, liver fat content is a novel independent indicator of myocardial insulin resistance and reduced coronary functional capacity. Further studies will reveal the effect of hepatic fat reduction on myocardial metabolism and coronary function.


2016 ◽  
Vol 37 (01) ◽  
pp. e5-e5
Author(s):  
J.-K. Cho ◽  
S.-U. Kim ◽  
H.-R. Hong ◽  
J.-H. Yoon ◽  
H.-S. Kang

Diabetes Care ◽  
2013 ◽  
Vol 37 (1) ◽  
pp. 242-251 ◽  
Author(s):  
Niina Matikainen ◽  
Leonie H. Bogl ◽  
Antti Hakkarainen ◽  
Jesper Lundbom ◽  
Nina Lundbom ◽  
...  

Obesity ◽  
2007 ◽  
Vol 15 (8) ◽  
pp. 1903-1907 ◽  
Author(s):  
Nancy A. Crimmins ◽  
Jessica G. Woo ◽  
Ritesh D. Kaushal ◽  
Ranjan Deka ◽  
Lawrence M. Dolan ◽  
...  

2009 ◽  
Vol 6 (9) ◽  
pp. 79-82
Author(s):  
Tomohiko Urano ◽  
Masataka Shiraki ◽  
Ryonosuke Yamaga ◽  
Noriko Sasaki ◽  
Yasuyoshi Ouchi ◽  
...  

Diabetes ◽  
2004 ◽  
Vol 53 (8) ◽  
pp. 2132-2136 ◽  
Author(s):  
H. Wang ◽  
H. Zhang ◽  
Y. Jia ◽  
Z. Zhang ◽  
R. Craig ◽  
...  

2013 ◽  
Vol 62 (4) ◽  
pp. 347-360 ◽  
Author(s):  
Bing-Hsien Liu ◽  
Yuan-Yu Lin ◽  
Ya-Chin Wang ◽  
Chao-Wei Huang ◽  
Chih-Chien Chen ◽  
...  

2015 ◽  
Vol 36 (13) ◽  
pp. e24-e30 ◽  
Author(s):  
J.-K. Cho ◽  
S.-U. Kim ◽  
H.-R. Hong ◽  
J.-H. Yoon ◽  
H.-S. Kang

AbstractLittle is known regarding whether adiponectin receptors mediate high-intensity interval training (HIT)-induced improvement of insulin resistance associated with obesity. This study investigated the effect of HIT on whole body insulin resistance in high-fat diet-induced obese mice. 5-week-old male mice (N=30) were randomly assigned to standard chow (SC) (n=10) or HFD (n=20) for 23 weeks. After 15 weeks of dietary treatment, the HFD mice were further assigned to HFD (n=10) or HFD plus HIT (HFD+HIT, n=10). The HFD+HIT mice were subjected to HIT during the last 8 weeks of the 23-week HFD course. HFD resulted in whole body insulin resistance, hypoadiponectinemia, suppressed expression of adiponectin receptor 1(AdipoR1) and 2 (AdipoR2), suppressed expression of phosphorylated AMP-activated protein kinase (p-AMPK) and NAD-dependent deacetylase sirtuin-1 (SIRT1), and decreased mRNAs of peroxisome proliferator-activated receptor-α (PPARα), carnitine palmitoyltransferase I (CPT1), and acyl CoA oxidase (ACO) in skeletal muscle. In contrast, HIT alleviated whole body insulin resistance and prevented decreased levels of total adiponectin in both serum and adipose tissue. HIT also prevented the down-regulation of AdipoR1 and AMPK/SIRT1 proteins and the down-regulation of PPARα, CPT1, and ACO mRNAs. The current findings show that HIT alleviates whole body insulin resistance due to HFD-induced obesity via the AdipoR1 and AMPK/SIRT1 mediated-signaling pathway in skeletal muscle, implying the potential role of HIT to combat this metabolic condition.


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