The Endocrinology of Anorexia Nervosa and Bulimia Nervosa

Newman, Michael M.; Halmi, Katherine A.

doi:10.1016/s0733-8619(18)30892-2

Cited by 27 publications

(23 citation statements)

References 122 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…[1][2][3] In addition, patients with AN have several endocrine abnormalities. These include abnormalities of the growth hormone (GH)-insulin-like growth factor 1 (IGF-1) axis 4,5 as well as decreased serum estrogen levels due to dysfunction of the hypothalamic-pituitary-gonadal axis 6,7 that leads to amenorrhea, anovulation, vaginal and breast atrophy.2,3 Based on the notion that initiation and maintenance of menstrual cycles would require the presence of a minimum amount of body fat to ensure adequate energy stores needed to sustain pregnancy and provide nutrition to the fetus, it has been previously proposed that the abnormal hypothalamicpituitary-gonadal function in anorexia nervosa could be the result of excessive weight loss. 8,9 Until recently this hypothesis remained unproven however, since the potential molecular link between decreased adipose stores and the hypothalamic-pituitary-gonadal axis had not been identified.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Leptin in relation to resumption of menses in women with anorexia nervosa

et al. 1998

View full text Add to dashboard Cite

Serum levels of leptin are decreased in underweight AN patients and increase with weight restoration. To assess the relationship of decreased leptin levels with other hormonal abnormalities in AN and to evaluate the possible role of increasing leptin levels, alone or in combination with other hormones, in the resumption of menses that accompanies weight gain, we studied crosssectionally sixty-five consecutively enrolled AN patients. Subjects were divided in three groups: (I) underweight and amenorrheic; (II) weight-recovered but still amenorrheic; and (III) weight-recovered and eumenorrheic women. Patients in group I had decreased BMI, serum leptin, estradiol (E2), insulin-like growth factor 1 (IGF-1) and urinary growth hormone (GH) levels and increased sex hormone-binding globulin (SHBG) levels, compared to AN patients in groups II and III. Moreover, although no differences in leptin levels or BMI were observed between amenorrheic and eumenorrheic weight-recovered patients (groups II and III), free E2 and GH levels were higher (PϽ0.02) in weight-recovered, eumenorrheic women. Thus, it appears that leptin is a necessary, but not a sufficient, factor for the resumption of menses in AN patients.Anorexia nervosa (AN) is a disorder characterized by abnormally low body weight, amenorrhea and specific psychopathologic features including intense fear of gaining weight and an abnormal way one's body weight, size or shape is perceived. [1][2][3] In addition, patients with AN have several endocrine abnormalities. These include abnormalities of the growth hormone (GH)-insulin-like growth factor 1 (IGF-1) axis 4,5 as well as decreased serum estrogen levels due to dysfunction of the hypothalamic-pituitary-gonadal axis 6,7 that leads to amenorrhea, anovulation, vaginal and breast atrophy.2,3 Based on the notion that initiation and maintenance of menstrual cycles would require the presence of a minimum amount of body fat to ensure adequate energy stores needed to sustain pregnancy and provide nutrition to the fetus, it has been previously proposed that the abnormal hypothalamicpituitary-gonadal function in anorexia nervosa could be the result of excessive weight loss. 8,9 Until recently this hypothesis remained unproven however, since the potential molecular link between decreased adipose stores and the hypothalamic-pituitary-gonadal axis had not been identified.Our understanding of the interaction between adipose stores and the reproductive system was recently greatly advanced by the discovery of leptin, 10 an adipocyte secreted hormone, whose circulating levels are directly associated with the amount of energy stored as fat. Leptin is the signal by which information about the amount of energy stores is conveyed to the brain, and thus, influences food intake and energy expenditure. 11In addition, a much broader spectrum of activities for this hormone has been recently suggested.11,12 More specifically, it has been proposed that leptin regulates several neuroendocrine axes, including the hypothalamic-pituitary-gonadal axis. 11...

show abstract

mentioning

confidence: 99%

mentioning

confidence: 99%

Leptin in relation to resumption of menses in women with anorexia nervosa

et al. 1998

View full text Add to dashboard Cite

show abstract

“…In this context, the study of chronic undernourished AN patients, with low plasma levels of endogenous estrogen and without estrogen replacement therapy, represents a useful approach for evaluating the effects of endogenous alteration of pulsatile GnRH secretion on gonadotropin isoform secretion. The present paper is the first to show in humans a relationship between GnRH, amenorrhea, nutrition and body weight, although their exact roles remain to be defined (2,3). Previous experiments have been performed on prepubertal animal models before the development of a mature reproductive system dependent on exogenous nutritional manipulations.…”

Section: Discussionmentioning

confidence: 91%

“…Although a clear relationship exists between menstrual dysfunction, weight loss and malnutrition, amenorrhea can predate weight loss and may persist despite weight gain (2,3). An abnormality in the central regulation of the gonadotropin-releasing hormone (GnRH) pulse-generation system has been described in both undernourished animal models (4)(5)(6) and humans with AN, with a reduced gonadotropin pulsatility and an age-inappropriate gonadotropin secretion pattern (3,(7)(8)(9)(10). Pulsatile GnRH therapy in AN patients has been reported to induce the quantitative restoration of both episodic luteinizing hormone (LH) secretion and pituitary LH responsiveness to GnRH (11).…”

Section: Introductionmentioning

confidence: 99%

Changes in the glycosylation pattern of circulating gonadotropins after acute administration of gonadotropin-releasing hormone in patients with anorexia nervosa

Savastano

Tommaselli²,

Valentino³

et al. 1998

European Journal of Endocrinology

View full text Add to dashboard Cite

To study the involvement of gonadotropin-releasing hormone (GnRH) in glycosylation of circulating gonadotropin isoforms in anorexia nervosa (AN), 14 amenorrhoic patients with AN, 14 age-matched volunteers in early follicular phase, and five normal-weight re-fed patients with AN were investigated under baseline conditions and after acute administration of GnRH. Plasma gonadotropins were assayed using IRMA before and after concanavalin A affinity chromatography. Baseline plasma gonadotropin levels were lower for both AN and re-fed AN patients than in controls (P<0.005). The increase in FSH and LH after GnRH administration was lower than in controls for AN (P<0.005) and re-fed AN (P<0.005 and P<0.05 respectively) patients. Percentages of total gonadotropin not bound to concanavalin A (complex carbohydrate chains) under baseline conditions were higher in patients with AN than in controls (P<0.005) but decreased after GnRH administration (P<0.001). In re-fed AN patients, the percentage of unbound FSH was higher than in controls (P<0.05), and decreased after GnRH administration (P<0.001), whereas the percentages of unbound LH were not significantly different from controls either before or after GnRH administration. These data suggest that: (a) the acute administration of GnRH induces quantitative and qualitative changes in circulating gonadotropin isoforms in both normal controls and AN patients; (b) during recovery the LH response in re-fed AN patients is associated with a glycosylation pattern that is the same as that for controls. European Journal of Endocrinology 138 76-81

show abstract

“…I for review]. The mechanisms underlying these events are poorly understood, though a large body of evidence indicates the existence in AN of a hypotha lamic dysfunction [2], which may account for the altered GH response pattern. It is still unclear whether the hypothalamic Received: July 12, 1990 Accepted after revision: October 4, 1990 dysfunction is the cause of AN or instead is a secondary, illnessrelated event.…”

mentioning

confidence: 99%

Studies of Growth Hormone Secretion in Calorically Restricted Dogs: Effect of Cholinergic Agonists and Antagonists, Glucose and Thyrotropin-Releasing Hormone

Arce¹,

Cella²,

Locatelli³

et al. 1991

Neuroendocrinology

View full text Add to dashboard Cite

The effect of caloric restriction (CR) on the growth hormone (GH) response to compounds reportedly capable of acting via somatostatinergic influences, i.e. cholinergic agonist or antagonist drug, glucose or thyrotropin-releasing hormone (TRH), administered alone or combined with GH-releasing hormone (GHRH), was evaluated in dogs. Eight beagle dogs, aged 4–5 years, underwent a 26-day period of increasing CR; they were evaluated either under basal conditions or starting from day 13 of CR, according to a schedule which allowed the mean length of CR to be similar among individual tests. CR resulted in a significant increase in basal GH levels, and starting from day 13 in a significant decrease in plasma somatomedin C levels; plasma glucose levels were significantly diminished on day 13 of CR and then remained unaltered. Administration of GHRH (GHRH1–44, 2 µg/kg, i.v.) induced a rise in plasma GH levels strikingly higher during CR than under basal conditions. Pyridostigmine (2 mg/kg orally), a muscarinic cholinergic agonist reportedly capable of restraining hypothalamic release of somatostatin (SS), enhanced the GH response to GHRH under basal conditions, but failed to do so during CR. Conversely, pirenzepine (0.6 mg/kg, i.v.), a muscarinic cholinergic antagonist, abolished the GHRH-induced GH rise under basal conditions, but only reduced it during CR. Only by doubling the dose of pirenzepine was complete inhibition of the GHRH-induced GH rise effected. Glucose alone (2 g/kg, p.o.) failed to modify basal GH secretion either before or during CR, but significantly inhibited the GHRH-induced GH rise either before or during CR. TRH (5 µg/kg, i.v.) did not modify plasma GH levels under basal conditions, but partially counteracted the rise in plasma GH occurring during CR. Like glucose, TRH significantly inhibited the GHRH-induced GH rise either before or during CR. Neither glucose nor TRH alone induced a ‘paradoxical’ rise in plasma GH during CR. In summary, (1) the data obtained with drugs affecting cholinergic transmission suggest that the latter is increased in dogs during CR and this likely results in a reduced hypothalamic SS tone, and (2) the data obtained with glucose and TRH suggest that these compounds may be effective to trigger not only hypothalamic SS release but also synthesis or, alternatively, they may act via inhibitory influences other than SS.

show abstract

The Endocrinology of Anorexia Nervosa and Bulimia Nervosa

Cited by 27 publications

References 122 publications

Leptin in relation to resumption of menses in women with anorexia nervosa

Leptin in relation to resumption of menses in women with anorexia nervosa

Changes in the glycosylation pattern of circulating gonadotropins after acute administration of gonadotropin-releasing hormone in patients with anorexia nervosa

Studies of Growth Hormone Secretion in Calorically Restricted Dogs: Effect of Cholinergic Agonists and Antagonists, Glucose and Thyrotropin-Releasing Hormone

Contact Info

Product

Resources

About