Effect of Oral Glucose Administration on Rebound Growth Hormone Release in Normal and Obese Women: The Role of Adiposity, Insulin Sensitivity and Ghrelin

Pena-Bello, Lara; Pértega-Díaz, Sonia; Outeiriño-Blanco, Elena; García-Buela, Jesús; Tovar, Sulay; Sangiao‐Alvarellos, Susana; Diéguez, Carlos; Cordido, Fernando

doi:10.1371/journal.pone.0121087

Cited by 20 publications

(21 citation statements)

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“…Another potential mechanism may be HbA1c [39], however in the present article we could not find a significant influence of the HbA1c value on the resistance to TH indices. There is an important relationship between the GH-IGF-1 axis and obesity [8][9][10]40], and circulating GH modulates the thyroid axis. Circulating GH levels increased serum FT3 and decreased serum FT4 in humans [41].…”

Section: Discussionmentioning

confidence: 99%

“…Excess body fat is associated with endocrine alterations, including decreased GH secretion [8][9][10] and thyroid dysfunction [10,11]. Thyroid hormone levels have been reported to be normal, increased, and decreased in obese patients; this discrepancy probably reflects the fact that the patients were examined at different times and may differ in degree and type of obesity and metabolic complications [11][12][13][14].…”

Section: Introductionmentioning

confidence: 99%

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Central Resistance to Thyroid Hormones in Morbidly Obese Subjects Is Reversed after Bariatric Surgery-Induced Weight Loss

Juiz-Valiña

Cordido

Outeiriño-Blanco

et al. 2020

JCM

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Endocrine abnormalities are common in obesity, including altered thyroid function. The altered thyroid function of obesity may be due to a mild acquired resistance to the thyroid hormone. The aim of this study was to investigate the effect of weight loss after bariatric surgery (BS) on resistance to thyroid hormones in patients with extreme obesity compared with a control group. We performed an observational study evaluating patients with extreme obesity who underwent BS. We included 106 patients (83 women) and 38 controls (24 women). The primary endpoint was the thyrotroph thyroxine resistance index (TT4RI) and thyroid stimulating hormone (TSH) index (TSHRI). The parameters were studied before and after surgery. TSHRI and TT4RI were higher in the obese patients than in the control group. TT4RI and TSHI decreased significantly over time after surgery, with this decrease being associated with the excessive body mass index (BMI) loss and C-reactive protein (CRP). In extreme obesity, BS promotes a significant decrease in the increased TT4RI and TSHI. This decrease of TT4RI and TSHI is progressive over time after BS and significantly associated with excess BMI lost and CRP. Extreme obesity is characterized by a mild reversible central resistance to thyroid hormones.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Central Resistance to Thyroid Hormones in Morbidly Obese Subjects Is Reversed after Bariatric Surgery-Induced Weight Loss

Juiz-Valiña

Cordido

Outeiriño-Blanco

et al. 2020

JCM

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“…Nass et al [ 37 ] found that endogenous acylated ghrelin increases the amplitude of GH pulses. Ghrelin secretion is decreased in obesity [ 38 ] and this decrease could be responsible, at least partially, for the alteration of GH secretion observed in obese individuals [ 10 ]. The IGF-1 feedback mechanism is preserved in obesity.…”

Section: Discussionmentioning

confidence: 99%

“…Excess body fat is associated with endocrine alterations, including thyroid dysfunction, central resistance to thyroid hormones [ 7 , 8 ] and decreased growth hormone (GH) secretion [ 9 , 10 , 11 ]. The altered GH secretion of obesity can be reversed by body weight normalization [ 12 ].…”

Section: Introductionmentioning

confidence: 99%

Altered GH-IGF-1 Axis in Severe Obese Subjects is Reversed after Bariatric Surgery-Induced Weight Loss and Related with Low-Grade Chronic Inflammation

Juiz-Valiña

Pena-Bello

Cordido

et al. 2020

JCM

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Endocrine disorders are common in obesity, including altered somatotropic axis. Obesity is characterized by reduced growth hormone (GH) secretion, although the insulin-like growth factor-1 (IGF-1) values are controversial. The aim of this study was to evaluate the effect of weight loss after bariatric surgery in the GH–IGF-1 axis in extreme obesity, in order to investigate IGF-1 values and the mechanism responsible for the alteration of the GH–IGF-1 axis in obesity. We performed an interventional trial in morbidly obese patients who underwent bariatric surgery. We included 116 patients (97 women) and 41 controls (30 women). The primary endpoint was circulating GH and IGF-1 values. Circulating IGF-1 values were lower in the obese patients than in the controls. Circulating GH and IGF-1 values increased significantly over time after surgery. Post-surgery changes in IGF-1 and GH values were significantly negatively correlated with changes in C-reactive protein (CRP) and free T4 values. After adjusting for preoperative body mass index (BMI), free T4 and CRP in a multivariate model, only CRP was independently associated with IGF-1 values in the follow-up. In summary, severe obesity is characterized by a functional hyposomatotropism at central and peripheral level that is progressively reversible with weight loss, and low-grade chronic inflammation could be the principal mediator.

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“…In a multivariate analysis, ghrelin was the only predictor for fasting and peak GH levels following oral glucose load in women [16] (Fig. 1).…”

Section: Gh Response To Oral Glucose and To Chronic Hyperglycemiamentioning

confidence: 99%

Growth Hormone Response to Oral Glucose Load: From Normal to Pathological Conditions

Hage

Kamenický

Chanson³

2019

Neuroendocrinology

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The exact physiological basis of acute growth hormone (GH) suppression by oral glucose is not fully understood. Glucose-mediated increase in hypothalamic somatostatin seems to be the most plausible explanation. Attempts to better understand its underlying mechanisms are compromised by species disparities in the response of GH to glucose load. While in humans, glucose inhibits GH release, the acute elevation of circulating glucose levels in rats has either no effect on GH secretion or may be stimulatory. Likewise, chronic hyperglycemia alters GH release in both humans and rats nonetheless in opposite directions. Several factors influence nadir GH concentrations including, age, gender, body mass index, pubertal age, and the type of assay used. Besides the classical suppressive effects of glucose on GH release, a paradoxical GH increase to oral glucose may be observed in around one third of patients with acromegaly as well as in various other disorders. Though its pathophysiology is poorly characterized, an altered interplay between somatostatin and GH-releasing hormone has been suggested and a link with pituitary ectopic expression of glucose-dependent insulinotropic polypeptide receptor has been recently demonstrated. A better understanding of the dynamics mediating GH response to glucose may allow a more optimal use of the OGTT as a diagnostic tool in various conditions, especially acromegaly.

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Effect of Oral Glucose Administration on Rebound Growth Hormone Release in Normal and Obese Women: The Role of Adiposity, Insulin Sensitivity and Ghrelin

Cited by 20 publications

References 55 publications

Central Resistance to Thyroid Hormones in Morbidly Obese Subjects Is Reversed after Bariatric Surgery-Induced Weight Loss

Central Resistance to Thyroid Hormones in Morbidly Obese Subjects Is Reversed after Bariatric Surgery-Induced Weight Loss

Altered GH-IGF-1 Axis in Severe Obese Subjects is Reversed after Bariatric Surgery-Induced Weight Loss and Related with Low-Grade Chronic Inflammation

Growth Hormone Response to Oral Glucose Load: From Normal to Pathological Conditions

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