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Prolactin and growth hormone secretion in chemically induced and genetically obese mice
Abstract:
Experiments were performed to determine PRL and GH concentrations in mice rendered obese by chemical means and to compare these concentrations with those of mice obese as a result of genetic mutation. Basal levels of serum PRL and GH were generally lower in gold thioglucose (GTG) and bipiperidyl mustard (BPM)-treated obese mice compared with lean controls. In the pituitary gland, the hormonal changes varied from lower or unchanged levels of PRL and GH shortly after drug injection to very high concentrations of PRL (but not of GH) a year later. However, when the mice were challenged with perphenazine, a drug that causes prompt release of PRL, GTG and BPM-obese mice released 2-5 times as much PRL as did lean controls, suggesting an impairment in the hypothalamic control of PRL secretion in GTG/BPM-obese mice. Basal levels of PRL and GH in genetically obese (ob/ob) mice of both sexes were also lower than those in their lean relatives (?/+). This was true for both serum and pituitary concentrations of the two hormones, the only exception being pituitary GH concentrations in females which were higher than or equal to those of controls. However, unlike GTG and BPM-obese mice, genetically obese mice released very little PRL compared with their lean relatives when stimulated with perphenazine, which suggested an insufficiency of pituitary function in ob/ob mice. The results demonstrate abnormalities in the secretion of PRL and GH in obese mice of both types.
Insights
Obesity in mice, whether chemically or genetically induced, alters prolactin (PRL) and growth hormone (GH) levels. Chemically obese mice show impaired hypothalamic control, while genetically obese mice exhibit pituitary insufficiency.
Area of Science:
- Endocrinology
- Obesity Research
- Neuroendocrinology
Background:
- Obesity is linked to hormonal dysregulation.
- Understanding prolactin (PRL) and growth hormone (GH) secretion in obesity is crucial.
Purpose of the Study:
- To compare PRL and GH concentrations in chemically and genetically obese mice.
- To investigate the impact of obesity on hypothalamic and pituitary function related to PRL and GH secretion.
Main Methods:
- Inducing obesity in mice using gold thioglucose (GTG) and bipiperidyl mustard (BPM).
- Utilizing genetically obese (ob/ob) mice.
- Measuring serum and pituitary PRL and GH levels.
- Stimulating PRL release with perphenazine.
Main Results:
- Chemically obese mice (GTG/BPM) had lower basal PRL and GH, but exaggerated PRL release upon perphenazine challenge, indicating hypothalamic dysfunction.
- Genetically obese mice (ob/ob) also had lower basal PRL and GH, with blunted PRL release upon perphenazine challenge, suggesting pituitary insufficiency.
- Hormonal changes varied between acute and chronic post-treatment periods in chemically obese mice.
Conclusions:
- Obesity, regardless of cause (chemical or genetic), is associated with significant abnormalities in PRL and GH secretion.
- Different obesity models display distinct neuroendocrine defects, highlighting the complexity of obesity-related hormonal imbalances.