Impaired Prolactin Secretion and Body Fat Distribution in Obesity

Abstract

Human obesity shows clustering within families. The hypothesis for the presence of a major gene or genes acting in human obesity is supported by recent evidence from studies of obesity in adoptees and their biological parents and siblings. The heterogeneity of obesity may be demonstrated by the shape of fat distribution and the prolactin response to insulin hypoglycaemia. Fat distribution has been shown to have a genetic background whereas a primary disorder of hypothalamic function is suspected in obese women who show an impaired prolactin response to insulin-induced hypoglycaemia. We have investigated the possible association between fat distribution and hypothalamic function in 23 extremely obese, nondiabetic premenopausal women who have been characterized using their absolute body weight, body mass index (BMI), fat distribution (expressed as waist to hip ratio), fasting insulin, basal prolactin and prolactin response to hypoglycaemia. Fasting insulin values showed a significant correlation (P less than 0.05, R = 0.604) with increasing waist to hip ratio (upper body segment obesity), whereas the graded prolactin response to hypoglycaemia of the obese women showed a negative association with increasing upper body segment obesity (P less than 0.05; R = -0.446). No relationship was observed between fasting insulin and the prolactin response to hypoglycaemia. We suggest that this previously unrecognized association of an impaired prolactin response to hypoglycaemia and upper body segment fatness may be useful for the investigation of the genetics of obesity.

Obese patients with obstructive sleep apnoea syndrome show a peculiar alteration of the corticotroph but not of the thyrotroph and lactotroph function

“…Finally, our results do not show any alteration of either thyrotroph or lactotroph function, in agreement with some but not other studies; in fact, some derangement in TSH or PRL secretion in obesity with or without OSAS has been demonstrated after administration of different stimuli, such as arginine or insulininduced hypoglycaemia (Clark et al, 1979;Kopelman et al, 1979;Cavagnini et al, 1981;Chomard et al, 1985;Grunstein et al, 1989;Weaver et al, 1990;Bratel et al, 1999;Roti et al, 2000).…”

“…These would reflect changes in body composition as they are usually reversed by weight loss (Kopelman et al ., 1979;Cavagnini et al ., 1981;Weaver et al ., 1990;Lin et al ., 1994;Winkelman et al ., 1996;Kopelman, 2000). These would reflect changes in body composition as they are usually reversed by weight loss (Kopelman et al ., 1979;Cavagnini et al ., 1981;Weaver et al ., 1990;Lin et al ., 1994;Winkelman et al ., 1996;Kopelman, 2000).…”

“…Simple obesity is also associated with some derangement in prolactin secretion and thyroid axis function. These would reflect changes in body composition as they are usually reversed by weight loss (Kopelman et al ., 1979;Cavagnini et al ., 1981;Weaver et al ., 1990;Lin et al ., 1994;Winkelman et al ., 1996;Kopelman, 2000). Studies on PRL secretion and thyroid axis in OSAS provided conflicting results (Clark et al ., 1979;Grunstein et al ., 1989;Lin et al ., 1994;Winkelman et al ., 1996;Bratel et al ., 1999).…”

The effects of hyperprolactinemia on bone and fat

“…On positron emission tomography obese individuals have decreased availability of striatal dopamine D2 receptors in inverse proportion to body mass index, and it has been postulated that dopamine deficiency perpetuates pathological eating behaviors in these individuals [53]. Obese subjects have a blunted prolactin response to insulin-induced hypoglycemia, thyrotropin releasing hormone, and metoclopramide [54][55][56][57][58][59] and in a subgroup of patients the abnormality persists after significant weight loss [60]. All of these findings suggest possible dysregulation of hypothalamic-pituitary function in obesity.…”

Neuroendocrine Alterations in Obese Patients with Sleep Apnea Syndrome

“…In human physiology, outside pregnancy, PRL secretion is altered by increasing body weight in both children and adults [81]. PRL in this circumstance appears to be a marker of hypothalamus-pituitary function: the PRL response to insulin-hypoglycaemia, Thyrotropin-Releasing Hormone (TRH) stimulation, and other stimulatory factors may be diminished [81–83]. In addition, obesity alters the 24 hour spontaneous release of PRL with a generalised dampening of release.…”