Glucose relays information regarding nutritional status to the neural circuits that control the somatotropic, corticotropic, and gonadotropic axes in adult male rhesus macaques

• Published in: Endocrinology (Philadelphia) Vol. 143; no. 2; pp. 403 - 410
• Main Authors: Lado-Abeal, Joaquin, Veldhuis, Johannes D, Norman, Reid L
• Format: Journal Article
• Language: English
• Published: United States 01.02.2002
• Subjects: Adrenocorticotropic Hormone - biosynthesis; Animals; Blood Glucose - physiology; Energy Metabolism - drug effects; Entropy; Fasting - physiology; Glucose - administration & dosage; Glucose - pharmacology; Gonadotropins - biosynthesis; Growth Hormone - biosynthesis; Injections, Intravenous; Luteinizing Hormone - biosynthesis; Luteinizing Hormone - blood; Macaca mulatta; Male; Mice; Nerve Net - physiology; Nutritional Status - physiology; Time Factors
• ISSN: 0013-7227; 1945-7170
• DOI: 10.1210/en.143.2.403

In male mammals, the neuroendocrine responses to fasting include increased GH and cortisol secretion and suppressed LH and T levels. Because blood glucose levels fall during fasting, we hypothesized that this modest, but consistent, change in blood glucose was a metabolic signal for the neuroendocrine adjustments of reproductive and metabolic hormones. Glucose (D-dextrose, 480 kcal/d) was infused into fasted (48 h) adult male rhesus macaques; and LH, cortisol, and GH were measured in plasma from samples collected at 15-min intervals for the last 15 h of the fast. We analyzed hormone secretion by deconvolution analysis, and the orderliness of release patterns by the approximate entropy statistic. Circulating blood glucose was 76 +/- 7 mg/dl in the fed control group, significantly higher (P < 0.01) than the level of 56 +/- 3 mg/dl in the fasted group. The increase in GH pulsatility and the 2-fold elevation in cortisol levels observed in the fasted male macaques were prevented by parenteral glucose delivery. The suppression of LH in fasted animals was not relieved by glucose infusions but seemed to be partially prevented in three of the animals. These findings are consistent with the hypothesis that glucose serves as a signal of nutritional status controlling adaptive neuroendocrine responses to fasting in the primate.