ArticleThe Biochemical journal1992
Regulation of cardiac adenylate cyclase activity in rodent models of obesity.
Article in The Biochemical journal, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 24 citations in OpenAlex.
- Saturated high-fat diet-induced obesity increases adenylate cyclase of myocardial β-adrenergic system and does not compromise cardiac function.Physiological reports · 2016Article
- Increased haemodynamic adrenergic load with isoflurane anaesthesia in type 2 diabetic and obese rats in vivo.Cardiovascular diabetology · 2014Article
- ACE-inhibition, but not weight reduction restores cardiomyocyte response to β-adrenergic stimulation in the metabolic syndrome.BMC cardiovascular disorders · 2013Article
- Leptin repletion restores depressed {beta}-adrenergic contractility in ob/ob mice independently of cardiac hypertrophy.The Journal of physiology · 2005Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have investigated beta-adrenergic regulation of adenylate cyclase activity in heart tissue membranes from the genetically obese Zucker rat, the genetically obese CBA mouse and the genetically obese diabetic (db/db) mouse. Responsiveness to beta-adrenergic stimulation was impaired in membranes from the obese Zucker rat, but not in the other models. The membranes from obese Zucker rats showed both decreased beta-adrenergic-receptor number and altered coupling between beta-adrenergic receptors and the stimulatory guanine-nucleotide-binding protein, Gs. In contrast, no alterations in either the levels of Gs or the functional interaction between this protein and the catalytic moiety of adenylate cyclase were observed. In these three genetic models of obesity we observe dissimilar alterations in the control of adenylate cyclase.
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Registered trials
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