Metabolic effects of vasopressin infusion in the starved rat. Reversal of ketonaemia
Open accessAbstract
The effects of vasopressin on the metabolism of starved rats were investigated by using a constant-infusion regimen (50 pmol/kg body wt. per min, after an initial loading dose of 150 pmol/kg body wt.). 2. Blood ketone bodies decreased by 50% in 10 min, and this was accompanied by a 60% decrease in the plasma non-esterified fatty acids. 3. Blood glucose increased by 0.9 mM within 5 min and decreased to control values over the 40 min infusion. Small increases in lactate and pyruvate also occurred. 4. Plasma insulin was not increased by vasopressin infusion. 5. The net decrease in blood ketone bodies caused by vasopressin was similar when somatostatin was infused simultaneously (1 nmol/kg body wt. per min). 6. Hepatic ketone bodies were significantly decreased by vasopressin, as was the 3-hydroxybutyrate/acetoacetate ratio. A small increase in the hepatic concentration of several glycolytic intermediates also occurred. 7. Vasopressin did not decrease the ketonaemia produced by infusions of octanoate or long-chain triacylglycerol in rats that had been pre-treated with the anti-lipolytic agent 3,5-dimethylpyrazole. 8. In comparison with vasopressin, the infusion of adrenaline or glucose had much smaller effects in decreasing the ketonaemia of starvation, despite the 4-fold increase in plasma insulin, at 10 min, with the glucose infusion. 9. The primary metabolic effect of vasopressin in the starved rat appears to be that of decreased supply of non-esterified fatty acid to the liver. It is suggested that vasopressin has a direct anti-lipolytic effect in adipose tissue.
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Acute vasopressin infusion in rats and healthy individuals causes a transient rise in blood glucose.
“Acute VP infusion in the rat and in healthy individuals was shown to induce a transient rise in blood glucose concentration [4][5][6].”
From Vasopressin and hydration play a major role in the development of glucose intolerance and hepatic steatosis in obese rats (2015) · cites this paper as [5]
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- Authors
- Rofe, A. M., & Williamson, D. H.
- Affiliations
- South Australia Pathology (AU)
- Venue
- Biochemical Journal
- Publisher
- Portland Press Ltd.
- Published
- 1983-04-15
- Volume
- 212
- Issue
- 1
- Pages
- 231-239
- ISSN
- 0264-6021 (ISSN-L)
- PMC
- PMC1152034
- OpenAlex
- W1694055304
- Cited by
- 65
- References
- 47
- Citations by year
- 2026: 1 · 2024: 2 · 2023: 3 · 2022: 1 · 2021: 1 · 2019: 3 · 2017: 1 · 2016: 3 · 2015: 1 · 2013: 1 · 2012: 1
- FWCI
- 2.39
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Biochemical Journal (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Lipid metabolism and biosynthesis
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Keywords
- vasopressin, starvation, ketonaemia, ketone bodies, free fatty acids, hepatic ketogenesis, adipose tissue lipolysis, somatostatin, insulin, epinephrine, glucose infusion, beta-hydroxybutyrate, acetoacetate, glycolytic intermediates, octanoate, 3,5-dimethylpyrazole
- MeSH terms
- Animals, Epinephrine, Glucose, Infusions, Parenteral, Ketone Bodies, Liver, Male, Rats, Inbred Strains, Somatostatin, Starvation, Vasopressins, Lipid Metabolism, Rats
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