Effect of acute reduction of free fatty acids by acipimox on growth hormone‐releasing hormone‐induced GH secretion in type 1 diabetic patients

Álvarez, P.; Isidro, Luisa; Peinó, R.; Leal‐Cerro, Alfonso; Casanueva, Felipe F.; Diéguez, Carlos; Cordido, Fernando

doi:10.1046/j.1365-2265.2003.01846.x

Cited by 7 publications

(4 citation statements)

References 43 publications

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“…There are controversial findings in the literature about stimulated GH values in patients with T1DM. Both normal responsiveness and enhanced responsiveness to several stimuli, such as GHRH and hexarelin, have been reported [17][18][19]22,23,26,28]. We have previously shown that GH responses to GHRH and GHRP-6 are similar in T1DM and in healthy subjects [20].…”

Section: Introductionmentioning

confidence: 75%

“…Nine healthy subjects (6 men and 3 women) were also studied as a control group. Their mean age was 28.4 ± 1.5 years (range, [20][21][22][23][24][25][26][27][28][29][30][31][32][33][34][35], and their mean BMI was 23.3 ± 0.8 kg/m 2 (range, 18.8-25.9). Mean HbA 1c was of 5.0% ± 0.1%.…”

Section: Subjectsmentioning

confidence: 99%

“…In patients with type 1 diabetes mellitus (T1DM), basal GH levels are either normal [17][18][19][20][21][22] or elevated [23][24][25], depending on glycemic control; and insulin-like growth factor-I (IGF-I) levels are normal [20] or reduced [19,21,[24][25][26]. It has been suggested that the enhanced GH secretion might be due to a decrease in IGF-I feedback on the hypothalamic-pituitary unit [27].…”

Section: Introductionmentioning

confidence: 99%

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Effects of ghrelin, growth hormone–releasing peptide–6, and growth hormone–releasing hormone on growth hormone, adrenocorticotropic hormone, and cortisol release in type 1 diabetes mellitus

et al. 2010

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In type 1 diabetes mellitus (T1DM), growth hormone (GH) responses to provocative stimuli are normal or exaggerated, whereas the hypothalamic-pituitary-adrenal axis has been less studied. Ghrelin is a GH secretagogue that also increases adrenocorticotropic hormone (ACTH) and cortisol levels, similarly to GH-releasing peptide-6 (GHRP-6). Ghrelin's effects in patients with T1DM have not been evaluated. We therefore studied GH, ACTH, and cortisol responses to ghrelin and GHRP-6 in 9 patients with T1DM and 9 control subjects. The GH-releasing hormone (GHRH)-induced GH release was also evaluated. Mean fasting GH levels (micrograms per liter) were higher in T1DM (3.5 ± 1.2) than in controls (0.6 ± 0.3). In both groups, ghrelin-induced GH release was higher than that after GHRP-6 and GHRH. When analyzing Δ area under the curve (ΔAUC) GH values after ghrelin, GHRP-6, and GHRH, no significant differences were observed in T1DM compared with controls. There was a trend (P = .055) to higher mean basal cortisol values (micrograms per deciliter) in T1DM (11.7 ± 1.5) compared with controls (8.2 ± 0.8). No significant differences were seen in ΔAUC cortisol values in both groups after ghrelin and GHRP-6. Mean fasting ACTH values were similar in T1DM and controls. No differences were seen in ΔAUC ACTH levels in both groups after ghrelin and GHRP-6. In summary, patients with T1DM have normal GH responsiveness to ghrelin, GHRP-6, and GHRH. The ACTH and cortisol release after ghrelin and GHRP-6 is also similar to controls. Our results suggest that chronic hyperglycemia of T1DM does not interfere with GH-, ACTH-, and cortisol-releasing mechanisms stimulated by these peptides.

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Section: Introductionmentioning

confidence: 75%

Section: Subjectsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Effects of ghrelin, growth hormone–releasing peptide–6, and growth hormone–releasing hormone on growth hormone, adrenocorticotropic hormone, and cortisol release in type 1 diabetes mellitus

et al. 2010

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“…Ghrelina, el ligando endógeno del receptor de los secretagogos de GH, probablemente desempeña también un papel 18 . Además, numerosos neurotransmisores, hormonas periféricas y señales metabólicas influyen en la secreción de GH 19 .…”

Section: Hipófisisunclassified

Función endocrina en la obesidad

Álvarez-Castro

Sangiao‐Alvarellos

Brandón-Sandá

et al. 2011

Endocrinología y Nutrición

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Obesity is associated to significant disturbances in endocrine function. Hyper insulinemia and insulin resistance are the best known changes in obesity, but their mechanisms and clinical significance are not clearly established. Adipose tissue is considered to be a hormone-secreting endocrine organ; and increased leptin secretion from the adipocyte, a satiety signal, is a well-established endocrine change in obesity. In obesity there is a decreased GH secretion. Impairment of somatotropic function in obesity is functional and may be reversed in certain circumstances. The pathophysiological mechanism responsible for low GH secretion in obesity is probably multifactorial. There are many data suggesting that a chronic state of somatostatin hypersecretion results in inhibition of GH release. Increased FFA levels, as well as a deficient ghrelin secretion, probably contribute to the impaired GH secretion. In women, abdominal obesity is associated to hyperandrogenism and low sex hormone-binding globulin levels. Obese men, particularly those with morbid obesity, have decreased testosterone and gonadotropin levels. Obesity is associated to an increased cortisol production rate, which is compensated for by a higher cortisol clearance, resulting in plasma free cortisol levels that do not change when body weight increases. Ghrelin is the only known circulating orexigenic factor, and has been found to be decreased in obese people. In obesity there is also a trend to increased TSH and free T3 levels.

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