Somatostatin release in response to glucose is impaired in chronic renal failure

Biomed Pharmacother. 1998;52(5):208-13. doi: 10.1016/S0753-3322(98)80018-8.

Abstract

In order to evaluate somatostatin (SRIH) secretion in uremia, plasma SRIH concentrations were determined in basal conditions and after an oral glucose tolerance test (OGTT) in 14 non-dialysed patients with chronic renal failure (CRF), seven of whom had normal glucose tolerance (NGT) and seven impaired glucose tolerance (IGT). Plasma insulin, C-peptide and glucagon and blood glucose concentrations were also evaluated. The results were compared with those obtained in a group of age- and sex-matched normal subjects. In CRF patients, plasma SRIH fasting values (8.6 +/- 0.6 and 7.8 +/- 0.6 pmol/L in NGT and IGT patients, respectively) were comparable to those recorded in controls (7.7 +/- 0.5 pmol/L). SRIH response to OGTT, evaluated as area under curves (AUC) above basal, was similar in both groups of CRF patients (412.9 +/- 84.5 and 415.6 +/- 51.9 pmol/L per min), and significantly lower than in controls (660.1 +/- 58.5 pmol/L per min). Data indicate that chronic uremia induces a loss of SRIH secretory cell responsiveness to glucose. A possible effect of impaired SRIH secretion on glucose metabolism in CRF is discussed.

MeSH terms

  • Adult
  • Aged
  • Blood Glucose / physiology*
  • C-Peptide / blood
  • Female
  • Glucagon / blood
  • Glucose Intolerance / blood*
  • Glucose Intolerance / physiopathology
  • Glucose Tolerance Test
  • Humans
  • Insulin / blood
  • Kidney Failure, Chronic / blood*
  • Kidney Failure, Chronic / physiopathology
  • Male
  • Middle Aged
  • Somatostatin / blood
  • Somatostatin / metabolism*
  • Uremia / blood
  • Uremia / physiopathology

Substances

  • Blood Glucose
  • C-Peptide
  • Insulin
  • Somatostatin
  • Glucagon