Year: 2015
Type: article
Abstract: Obesity has reached pandemic proportions with 1.9 billion overweight adults; 600 million of whom are obese [1]. It has been shown that stimulating cyclic 3’-5 ’ guanosine monophosphate (cGMP) signaling is able to promote adi-pose tissue homeostasis in obese mice [2]. Conversely, genetic depletion of cGMP dependent protein kinase 1 (PKG1), causes hepatic inflammation and fasting hypergly-cemia in mice [3]. Furthermore, cGMP signaling is essen-tial for differentiation of preadipocytes to mature adipocytes in vitro [4,5]. PKG1 activation blocks RhoA mediated inhibition of insulin receptor substrate 1 in adi-pocytes in vitro [4,5], thus maintaining insulin sensitivity. The status of cGMP signaling cascade in adipose tissue under obese conditions is not yet fully understood. Here, we examine the functional status of cGMP signaling in
Source: BMC Pharmacology and Toxicology
Institution: University of Bonn
Language: English
Subfield: Endocrinology, Diabetes and Metabolism
Field: Medicine
Domain: Health Sciences
Open Access status: gold
Estimated APC paid: $3,090
OpenAlex ID: W1850031619
