The Effect of Free Fatty Acids on Growth Hormone(GH)-Releasing Hormone-Mediated GH Secretion in Man*

Imaki, Toshihiro; Shibasaki, Tamotsu; Shizume, Kazuo; Masuda, Akitsugu; Hotta, Mari; Kiyosawa, Yoshino; Jibiki, Kazuko; Demura, Hiroshi; Tsushima, Takahiro; Ling, Nicholas

doi:10.1210/jcem-60-2-290

Cited by 167 publications

(64 citation statements)

References 19 publications

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“…18 A similar GH suppression by FFA was reported in rats. 19 Our data also show FFA plasma levels in obese pre-BPD subjects, signi®cantly higher than in normal weight ones.…”

Section: Discussionsupporting

confidence: 69%

“…22 Among peripheral factors, metabolic fuels could directly in¯uence the hypothalamic balance between stimulating and inhibition factors for GH. GH is not suppressed by oral glucose in obesity, 18 but the further increase after a meal could indicate not only a lack of inhibition, but rather an altered hypothalamic sensitivity to metabolites. Maccario et al 23 observed that while pirenzepine, a direct cholinergic drug, abolished the GH response to GHRH and arginine, as in normal humans, obese subjects differed from the controls with respect to glucose action; the GHRH-and arginineinduced GH release were refractory to the inhibitory effect of glucose.…”

Section: Discussionmentioning

confidence: 98%

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Evaluation of pre- and postprandial growth hormone (GH)-releasing hormone-induced GH response in subjects with persistent body weight normalisation after biliopancreatic diversion

Marinis¹,

Mancini²,

Valle

et al. 1998

Int J Obes

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BACKGROUND: Obesity is characterised by growth hormone (GH) abnormalities, including a blunted response to stimulation and a`paradoxical' increase after meals. The blunted GH release is reversed by a surgical intestinal bypass procedure. However, this does not mean that normal GH dynamics have been restored. The present study assessed whether post-surgical weight reduction in obese patients normalised the modulation of GH release produced by metabolic fuels. SUBJECTS: Ten obese female subjects, aged 23 ± 54 y, were studied before and after biliopancreatic diversion (BPD). All patients, after surgery, had experienced a signi®cant reduction in body weight (mean body mass index (BMI) 25.78 AE 1.01 kgam 2 vs 44.68 AE 1.73 kgam 2 ). Two groups were also studied as controls: Ten normal body weight female subjects and ten patients suffering from anorexia nervosa (AN, mean BMI 17.46 AE 1.12 kgam 2 ). MEASUREMENTS: We have studied the GH response to a GH releasing hormone (GHRH) bolus (1 m mgakg iv, at 13.00 h) before and after a standard meal. RESULTS: In post-BPD subjects, the GH response to GHRH in the fasting state, was clearly augmented in comparison with the pre-BPD values (peak values 18.06 AE 4.56 vs 3.24 AE 0.68 m mgaL). In post-BPD subjects the postprandial GH response was further augmented in comparison with the fasting test (peak 30.12 AE 4.99 m mgaL, P`0.05). This pattern was similar to that observed in anorexic patients. CONCLUSION: The surgical procedure restores a normal GH response to GHRH in the fasting state, but thè paradoxical' GH response after meals remains present, suggesting a persistent GH derangement in such patients, which is not related to body weight per se. The surgical procedure makes obese patients similar to anorexics, in the relationships between metabolic fuels and GH secretion. The persistence of the GH postprandial response to GHRH in post-BPD subjects suggests a role for metabolic fuels in the regulation of somatostatin (SRIF) secretion.

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“…18 A similar GH suppression by FFA was reported in rats. 19 Our data also show FFA plasma levels in obese pre-BPD subjects, signi®cantly higher than in normal weight ones.…”

Section: Discussionsupporting

confidence: 69%

Section: Discussionmentioning

confidence: 98%

Evaluation of pre- and postprandial growth hormone (GH)-releasing hormone-induced GH response in subjects with persistent body weight normalisation after biliopancreatic diversion

Marinis¹,

Mancini²,

Valle

et al. 1998

Int J Obes

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show abstract

“…FFA elevations reduce or block GH secretion stimulated by a variety of stimuli or conditions, such as FFA depression, hypoglycemia, physical exercise or administration of GH releasing hormone (GHRH) or GHRP-6. 3,4 There is now compelling evidence indicating that the FFA blockade of GH secretion is exerted at the pituitary level, probably by direct inhibition of somatotroph function. 4,5 The effect of FFA on GH secretion is exerted at physiological levels, since reduction in circulating FFA levels following administration of acipimox, per se stimulates basal GH secretion as well as increasing GH responses to different GH secretagogues in normal subjects.…”

Section: Free Fatty Acids and Gh Secretionmentioning

confidence: 99%

Regulation of somatotroph cell function by the adipose tissue

et al. 2000

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Obese subjects exhibit a marked decrease in plasma growth hormone (GH) levels. However, the mechanisms by which increased adiposity leads to an impairment of GH secretion are poorly understood. Recent evidence suggests that the adipose tissue can markedly in¯uence GH secretion via two different signals, namely free fatty acids (FFA) and leptin. FFA appear to inhibit GH secretion mainly by acting directly at pituitary level. Interestingly, reduction in circulating FFA levels in obese subjects led to a marked increase in GH responses to different GH secretagogues. This indicates that FFA exert a tonic inhibitory effect that contributes to blunted GH secretion in obese subjects. Recent data have shown that leptin is a metabolic signal that regulates GH secretion, since the administration of leptin antiserum to adult rats led to a marked decrease in spontaneous GH secretion. However, leptin prevents,the inhibitory effect exerted by fasting on plasma GH levels. The effect of leptin in adult rats appears to be exerted at hypothalamic level by regulating growth hormone releasing hormone (GHRH), somatostatin and neuropeptide Y (NPY)-producing neurones. In addition, during fetal life or following the development of pituitary tumors, leptin can also act directly at the anterior pituitary.

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“…The increased plasma FFA suppressed GRF-induced GH secretion in rats [27]. The plasma FFA increase induced by an intravenous infusion of lipid-heparin inhibited GH secretion in response to GRF in man [28]. In sheep, the intravenous infusion of FFA has also been reported to suppress the frequency of GH pulses and the GH response to GRF [29].…”

Section: Discussionmentioning

confidence: 99%

Inhibitory Effect of Volatile Fatty Acids on GRF-Induced GH Secretion in Sheep.

et al. 1993

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Abstract. The effect of intravenous infusion of acetate, propionate and butyrate (0, 3, 10, 30 µmol kg-' min-1 over 40 min) on the secretion of growth hormone (GH), insulin and glucagon in response to growth hormone-releasing factor (GRF) injection (0.25 µg/kg, 10 min after the onset of acid infusion) was determined in six sheep. The intravenous injection of GRF caused a marked increase in plasma GH at every dose of each acid. The GH response to GRF was unaffected by an intravenous infusion of acetate. The basal plasma levels of insulin, glucagon and glucose were unchanged by acetate infusion. The infusion of propionate markedly suppressed the GH response to GRF in a dose-dependent manner. Propionate produced increases in plasma insulin, glucagon and glucose concentrations. Butyrate infusion also caused a significant attenuation of GRF-induced GH secretion. Butyrate infusion stimulated the secretion of both insulin and glucagon and caused hyperglycemia. After cessation of the infusion of propionate or butyrate plasma GH tended to increase again. Plasma somatostatin concentrations, which were measured only for the highest dose of butyrate, were unchanged during acid infusion, but increased on discontinuing the infusion. It is concluded that propionate and butyrate suppress GH secretion, while stimulating the secretion of insulin and glucagon in sheep.Key words: Growth hormone, Volatile fatty acids, Growth hormone-releasing factor, Sheep.( the rumen is metabolized in the rumen epithelium to produce ketone bodies and the remainder is oxidized in the liver [3]. Thus a basic role of VFA in ruminants is to meet a large proportion of their energy needs.In addition to the importance of VFA as an energy source for the animal, some attention has been paid to the effects of VFA on the secretion of metabolic hormones such as insulin and glucagon. Manns and Boda [4] first reported that butyrate and propionate injected intravenously enhanced insulin secretion in sheep. These observations have been confirmed by other workers [5]. Infusions of butyrate or propionate into the portal vein of sheep at rates producing portal plasma concentrations within the range observed after feeding caused increased insulin secretion, suggesting a

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The Effect of Free Fatty Acids on Growth Hormone(GH)-Releasing Hormone-Mediated GH Secretion in Man*

Cited by 167 publications

References 19 publications

Evaluation of pre- and postprandial growth hormone (GH)-releasing hormone-induced GH response in subjects with persistent body weight normalisation after biliopancreatic diversion

Evaluation of pre- and postprandial growth hormone (GH)-releasing hormone-induced GH response in subjects with persistent body weight normalisation after biliopancreatic diversion

Regulation of somatotroph cell function by the adipose tissue

Inhibitory Effect of Volatile Fatty Acids on GRF-Induced GH Secretion in Sheep.

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