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Decreased prolactin secretion in childhood obesity
Insights
Childhood obesity is linked to impaired prolactin secretion. Obese children showed decreased prolactin responses to insulin and TRH tests, suggesting neuroendocrine regulation issues.
Area of Science:
- Endocrinology
- Pediatric Endocrinology
- Neuroendocrinology
Background:
- Childhood obesity is a growing public health concern.
- Obesity can affect hormonal regulation and endocrine function.
- Previous studies suggest potential neuroendocrine alterations in obese individuals.
Purpose of the Study:
- To investigate prolactin secretion in response to insulin and TRH in obese children.
- To compare hormonal responses between obese children and healthy controls.
- To explore potential neuroendocrine dysregulation in childhood obesity.
Main Methods:
- Twelve obese children and seven age/sex-matched controls underwent intravenous insulin and TRH tests.
- Serial measurements of prolactin, growth hormone, insulin, glucose, cortisol, glucagon, TSH, T4, and T3 were performed using RIA.
- Hormonal responses were analyzed between the obese and control groups.
Main Results:
- Obese patients had higher basal insulin levels and lower peak growth hormone responses to insulin compared to controls.
- Five of 12 obese children showed no prolactin response to insulin.
- Obese children exhibited significantly lower prolactin responses to both insulin and TRH stimuli compared to controls.
Conclusions:
- Prolactin secretion is decreased in childhood obesity following both insulin and TRH stimulation.
- The impaired prolactin response is more pronounced after insulin administration.
- Neuroendocrine regulation of prolactin release appears to be impaired in obese children, similar to adult hypothalamic obesity.
Abstract:
Twelve obese patients and 7 control subjects, age and sex matched, whose weights were greater than 200% of ideal weight and 100% of ideal body weight, respectively, underwent intravenous insulin and thyroid releasing hormone (TRH) tests. Serial prolactin growth hormone, insulin, blood sugar, cortisol, glucagon, thyrotropin stimulating hormone, thyroxine, and triiodothyronine were obtained by RIA. Obese patients showed no significant differences from controls in basal and nadir glucose, basal and peak glucagon, cortisol, and thyroid responses to both tests. Basal insulin levels were higher (36 +/- 9.4 vs 10 +/- 2.3 microU/ml, P less than 0.05) and peak growth hormone responses after insulin were lower in the obese group (6.1 +/- 1.1 vs 12.7 +/- 3.7 ng/ml, P less than 0.05) than in controls. Whereas all control subjects had prolactin responses to both tests, five of 12 obese patients had no responses to insulin. Obese patients had lower prolactin responses at 30 minutes after insulin (5.4 +/- 0.7 vs 12.9 +/- 3.7 ng/ml, P less than 0.05) and lower prolactin responses at 60 minutes after TRH (9.9 +/- 1.7 vs 20.4 +/- 5.9 ng/ml, P less than 0.05). Maximum prolactin responses after TRH were lower in obese patients (9.9 +/- 2.0 vs 28.8 +/- 10.9 ng/ml, P less than 0.05). Maximum prolactin responses after insulin were lower in obese patients (6.2 +/- 4.1 vs 28.9 +/- 18.3 ng/ml). Thus prolactin secretion in childhood obesity is decreased after both stimuli, but more so after IV insulin that TRH, and suggests that, as in adult hypothalamic obesity, neuroendocrine regulation of prolactin release in obese children is impaired.