Plasma Glucose and Free Fatty Acids Modulate the Secretion of Growth Hormone, but not Prolactin, in the Rhesus and Java Monkey*

Quabbe, Hans-Jürgen; Bunge, Stephan; Walz, Thomas; Bratzke, B

doi:10.1210/jcem-70-4-908

Cited by 10 publications

(5 citation statements)

References 34 publications

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“…Hypoglycemia induced by insulin stimulated the re lease of ACTH and (TEND but had no significant effect on PRL secretion, which confirms previous observations [38][39][40]. At the same time, insulin, without affecting the HA level, increased the hypothalamic content of r-meHA almost 2-fold, indicating that neuronal HA is released by insulin-induced hypoglycemia.…”

Section: Discussionsupporting

confidence: 88%

Responses of Anterior Pituitary Hormones and Hypothalamic Histamine to Blockade of Histamine Synthesis and to Selective Activation or Inactivation of Presynaptic Histamine H<sub>3</sub> Receptors in Stressed Rats

et al. 1993

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The stress-induced release of anterior pituitary hormones and changes in hypothalamic content of histamine (HA) and its metabolite tele-methylHA (t-meHA) were studied in male rats during inhibition of HA synthesis or activation or blockade of HA H₃ receptors. Pretreatment with the HA synthesis inhibitor α-fluoromethylhistidine (α-FMH; 200 µg intracerebroventricularly (icv) at –120 min) or the specific H₃ receptor agonist R(α)methylhistamine (RmHA; 10 mg/kg intraperitoneally (ip) at –180 and –60 min) inhibited by 30–80% the responses of prolactin (PRL), corticotropin (ACTH) and β-endorphin (β-END) immunoreactivity to 1, 2.5 or 5 min of restraint stress (p < 0.05–0.01), but had no effect on basal secretion of the hormones. The inhibitory effect of the H₃ receptor agonist RmHA (10 mg/kg × 2) on the hormone response to 5 min of restraint stress was prevented by simultaneous ip administration of the H₃ receptor antagonist thioperamide. α-FMH reduced the hypothalamic content of HA 60% and that of t-meHA 30%, while RmHA had no effect on the HA content. Restraint stress for 5 min did not affect the HA and t-meHA contents, which may be due to the short duration of stress exposure. Pretreatment with the H₃ receptor antagonist thioperamide (5 or 10 mg/kg ip at-120 min) had no effect on basal or restraint stress-induced release of PRL, ACTH or β-END, although the compound increased the hypothalamic content of t-meHA 2-fold. Insulin-induced (1 IU/kg ip) hypoglycemia increased the plasma concentration of ACTH and β-END 2- and 1.5-fold, respectively, and increased the hypothalamic content of t-meHA almost 2-fold, which indicates an increased turnover of neuronal HA. α-FMH or RmHA prevented the insulin-induced release of ACTH and β-END. Insulin had no significant effect on PRL secretion. In conclusion, the findings that the response of PRL, ACTH and α-END to stress or insulin-induced hypoglycemia was inhibited by blockade of HA synthesis or activation of H₃ receptors and that hypothalamic HA turnover increased in response to hypoglycemia further implicate a role of hypothalamic histaminergic neurons in the neuroendocrine regulation of pituitary hormone secretion.

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Section: Discussionsupporting

confidence: 88%

Responses of Anterior Pituitary Hormones and Hypothalamic Histamine to Blockade of Histamine Synthesis and to Selective Activation or Inactivation of Presynaptic Histamine H<sub>3</sub> Receptors in Stressed Rats

et al. 1993

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“…Sartin et al (5) reported recently that, in the ewe, decreased peripheral or central nervous system glucose availability antagonized the GRF-induced secretion of GH, while elevated plasma glucose concentrations had no effect. Similarly, in the monkey, hypoglycemia enhanced GH secretion and hyperglycemia had no effect (30). The apparent species differences by which hyperglycemia or The ruminant brain can utilize alternative energy sources (32) and may not require a rapid increase in glucose production after brain glucopenia.…”

Section: Discussionmentioning

confidence: 99%

“…This is in contrast to reports in the rat (7, 28), ewe (6). monkey (30), and human (8, 9), in which exogenous FFA administration decreased circulating concentrations of GH. The FFA treatment regime employed in Experiment 2 did not maintain serum FFA concentrations above control levels for the duration of the treatment period.…”

Section: Discussionmentioning

confidence: 99%

Serum Glucose and Free Fatty Acids Modulate Growth Hormone and Luteinizing Hormone Secretion in the Pig

Barb

Kraeling

Barrett

et al. 1991

Experimental Biology and Medicine

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Two experiments were conducted to determine the effect of free fatty acids (FFA) and glucose treatment on growth hormone (GH) and luteinizing hormone secretion in the pig. In Experiment (Exp) 1, 15 prepuberal gilts received an intravenous infusion of FFA (n = 5; 3 ml of 10% Liposyn II/kg), glucose (n = 5; 1 g/kg), or saline (n = 5; 3 ml of 0.9%/kg). Jugular blood samples were collected every 15 min for 2 hr before and 3 hr after intravenous infusion of saline, FFA, and glucose. Synthetic [Ala15]-h growth hormone-releasing factor-(1-29)NH2 (1 microgram/kg) and gonadotropin-releasing hormone (0.2 micrograms/kg) were administered 30 min after infusion (Time 0 = infusion). In Exp 2, eight prepuberal gilts received either FFA (n = 4) or saline (n = 4) as described in Exp 1, except that treatments were given every hour ove a 10-hr period. Blood samples were collected every 15 min from 1 hr before to 10 hr after the start of FFA or saline infusion. In Exp 1, the peak GH response to growth hormone-releasing factor was delayed by 45 min (P less than 0.01) by glucose treatment and suppressed (P less than 0.01) by FFA treatment. The luteinizing hormone response to gonadotroph-releasing hormone was suppressed (P less than 0.03) by glucose and enhanced (P less than 0.03) by FFA. In Exp 2, the number of GH pulses was increased (P less than 0.05) by FFA infusion and GH concentrations were positively correlated (r = 0.58, P less than 0.0003) with FFA concentrations, while luteinizing hormone pulse amplitude was greater (P less than 0.01) in FFA gilts than in saline gilts. These results indicate that FFA are more effective modulators of GH secretion than acute hyperglycemia, while metabolic status can alter pituitary responsiveness to gonadotropin-releasing hormone.

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“…Obesity is associated with high circulating free fatty acid (FFA) concentrations (11, 21), and FFA have been shown to suppress GH release in humans and animals (5,6,13,19,27,41). Thus hyposomatotropism in obese individuals may be brought about by elevated plasma FFAs.…”

mentioning

confidence: 99%

Acipimox enhances spontaneous growth hormone secretion in obese women

Kok

Buijs²,

Kok³

et al. 2004

American Journal of Physiology-Regulatory, Integrative and Comp

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We hypothesized that a high circulating free fatty acid (FFA) concentration is involved in the pathogenesis of hyposomatotropism associated with obesity. To evaluate this hypothesis, 10 healthy premenopausal women (body mass index 33.8 +/- 1.0 kg/m(2)) were studied in the follicular phase of their menstrual cycle at two occasions with a time interval of at least 8 wk, where body weight remained stable. Subjects were randomly assigned to treatment with either acipimox (an inhibitor of lipolysis, 250 mg orally 4 times daily) or placebo in a double-blind crossover design, starting 1 day before admission until the end of the blood sampling period. Blood samples were taken during 24 h with a sampling interval of 10 min for assessment of growth hormone (GH) concentrations, and GH secretion was estimated by deconvolution analysis. Identical methodology was used to study GH secretion in a historical control group of age-matched normal weight women. GH secretion was clearly blunted in obese women (total daily release 66 +/- 10 vs. lean controls: 201 +/- 23 mU x l(Vd)(-1) x 24 h(-1), P = 0.005, where l(Vd) is lite of distribution volume). Acipimox considerably enhanced total (113 +/- 50 vs. 66 +/- 10 mU x l(Vd)(-1) x 24 h(-1), P = 0.02) and pulsatile GH secretion (109 +/- 49 vs. 62 +/- 30 mU x l(Vd)(-1) x 24 h(-1), P = 0.02), but GH output remained lower compared with lean controls. Further analysis did not show any relationship between the effects of acipimox on GH secretion and regional body fat distribution. In conclusion, acipimox unleashes spontaneous GH secretion in obese women. It specifically enhances GH secretory burst mass. This might mean that lowering of systemic FFA concentrations by acipimox modulates neuroendocrine mechanisms that orchestrate the activity of the somatotropic ensemble.

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Plasma Glucose and Free Fatty Acids Modulate the Secretion of Growth Hormone, but not Prolactin, in the Rhesus and Java Monkey*

Cited by 10 publications

References 34 publications

Responses of Anterior Pituitary Hormones and Hypothalamic Histamine to Blockade of Histamine Synthesis and to Selective Activation or Inactivation of Presynaptic Histamine H<sub>3</sub> Receptors in Stressed Rats

Responses of Anterior Pituitary Hormones and Hypothalamic Histamine to Blockade of Histamine Synthesis and to Selective Activation or Inactivation of Presynaptic Histamine H<sub>3</sub> Receptors in Stressed Rats

Serum Glucose and Free Fatty Acids Modulate Growth Hormone and Luteinizing Hormone Secretion in the Pig

Acipimox enhances spontaneous growth hormone secretion in obese women

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