Abstract
This article is part of a themed section on Redox Biology and Oxidative Stress in Health and Disease. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v174.12/issuetoc.
Highlights
The majority of type 2 diabetes cases are related to insulin resistance and obesity (Anderson et al, 2003), suggesting a causal connection between these conditions (Berger, 1992; Daly, 1994)
When the inflows of nutrients into adipose tissues exceed the capability of adipocytes to handle nutrient excess and the capacity of adipose tissue to expand by hyperplasia, more adipocytes become hypertrophic and defend themselves by developing insulin insensitivity (Gray and Vidal-Puig, 2007)
Compared with the other insulin-sensitive tissues, such as liver and muscle, adipose tissue is less important for postprandial glucose clearance, and the energy for cellular functions in adipocytes is primarily obtained via glycolytic ATP production
Summary
TARGETS Enzymesa AMPK eNOS sGC, soluble guanylyl cyclase iNOS nNOS PDE3B PKB/Akt XO, xanthine oxidoreductase. Other proteinsd Fatty acid binding protein 4 PGC-1α, PPARγ coactivator 1α Transporterse UCP1, uncoupling protein 1, SLC25A7. These Tables list key protein targets and ligands in this article which are hyperlinked to corresponding entries in http://www.guidetopharmacology.org, the common portal for data from the IUPHAR/BPS Guide to PHARMACOLOGY (Southan et al, 2016) and are permanently archived in the Concise Guide to PHARMACOLOGY 2015/16 (a,b,c,d,e Alexander et al, 2015a,b,c,d,e)
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