• DOI:10.1042/BST0051162
• Corpus ID: 28620387

Adenylate Cyclase Activity in Hepatic Plasma Membranes from Obese-Hyperglycaemic Mice

@article{Dehaye1977AdenylateCA,
  title={Adenylate Cyclase Activity in Hepatic Plasma Membranes from Obese-Hyperglycaemic Mice},
  author={Jean Paul Dehaye and Jacques Winand and Jean Christophe},
  journal={Biochemical Society Transactions},
  year={1977},
  volume={5},
  pages={1162-1164}
}

• J. Dehaye, J. Winand, J. Christophe
• Published 1 August 1977
• Biology, Medicine
• Biochemical Society Transactions

In partially purified hepatic plasma membranes from obese-hyperglycaemic mice, the four sites of the adenylate cyclase system are intact : the hormone-receptor, the regulatory unit to guanyl nucleotides, the inhibitory site for adenosine, and the site for divalent cations. The catalytic unit of the enzyme is also unaltered. This suggests that the glucagon-sensitive hepatic adenylate cyclase remains normal in this syndrome. The obese-hyperglycaeraic syndrome of Bar-Harbor is characterized by obesity, hyperinsulinism and insulin résistance (Christophe et al., 1959). This triad has been correlated with a lack of insulin receptors on plasma membranes of cells as différent as adipocytes (Freychet et al., 1972), hepatocytes (Kahn et al., 1972) and thymocytes (Soll et al., 1974), Récent reports suggest further altérations in the plasma membranes of obese-hyperglycaemic (ob/ob) mice. First, it has been shown that the adenylate-cyclase activity of adipose tissue plasma membranes is reduced (Dehaye et al., 1976). This defect correlates well with very low élévations in cyclic AMP levels in response to lipolytic agents and may be responsible for the reduced lipolysis in adipose tissue from ob/ob mice (Dehaye et al., 1975 and 1977). Secondly, Chang et al. (1975) have shown that a more gênerai defect altering glycoproteins in a variety of plasma membranes is involved in this syndrome. Our purpose in this study was to investigate another typical plasma membrane system, the glucagon-sensitive hepatic adenylate cyclase, in order to see whether this membrane component is also modified in the ob/ob syndrome. C57 Bl 6J mice