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[Leptin and it's potential role in the pathomechanism of some hormonal and metabolic disorders of patients with anorexia nervosa].

AbstractUNLABELLED:
The obese gene product--leptin (LEP)--is a hormone released from adipose tissue implicated in the regulation of nutritional state and energy balance. The aim of this study was to assess the relationship between plasma LEP levels and nutritional state, secretion of hormones of the hypothalamic-pituitary axis, and personality traits in patients with anorexia nervosa (AN). The study was performed in 22 women with AN aged 19.45 +/- 0.92 yrs, mean BMI of 15.48 +/- 0.29 kg/m2, 14 healthy women with normal body weight (NW), aged 29.71 +/- 2.4 yrs, mean BMI of 21.22 +/- 0.43 kg/m2, and 19 obese women without metabolic disorders (OTY), aged 34.5 +/- 2.65 yrs, mean BMI of 37.47 +/- 2.06 kg/m2. Hormone levels were measured with RIA test kits. Psychological examination was carried out by means of Gough-Helibrun's and Catell's personality tests. Body mass index (BMI) and body composition, i.e. body fat mass (BF) and body fat percentage (%BF) were determined with a DEXA instrument (Lunar Co., WI, USA). Absolute plasma LEP levels and the LEP/%BF index were lowest in patients with AN whereas LEP/BF index did not differ among AN, NW, and OTY groups (Table 1). In all groups, LEP levels were positively correlated with BMI, BF, and %BF (Table 2). Plasma neuropeptide Y (NPY), beta-endorphin (B-EP), and galanin (GAL) levels in AN were significantly higher than in NW and OTY groups (Table 3). Plasma GAL levels were positively correlated with LEP/BF and LEP/%BF in AN patients only. Moreover in the AN group, serum/plasma levels of insulin (I), insulin-like growth hormone-1 (IGF-1), luteinizing hormone (LH), follicle stimulating hormone (FSH), estradiol (E2), and free triiodothyronine (fT3) were significantly lower, and levels of cortisol (F) significantly higher than in NW and OTY groups (Table 4). Plasma LEP levels in AN patients were positively correlated with IRI, IGF-1, free thyroxine (fT4), and FSH levels, and negatively correlated with thyrotrophin (TSH) levels. Personality traits in patients with AN were significantly correlated with hormone levels (Tables 5 and 6), BMI and body fat content (Table 6).
CONCLUSIONS:
1) Leptin secretion from adipose tissue is not related to the nutritional state. 2) High levels of NPY, beta-EP, and GAL in AN confirm that starvation is deliberate in these patients. Low LEP levels in AN may lead to secondary amenorrhea and thyroid function disorders, as well as enhanced cortisol and growth hormone secretion of hypothalamic origin. A positive correlation between levels of LEP and IGF-1 and IRI may reflect mechanisms preserving adipose tissue and protecting from hypoglycemia and insulin resistance. A positive correlation between LEP and fT4 levels suggests a tendency to energy-sparing under conditions of low energy intake. Lack of correlation between LEP and F levels apparently reflects peripheral cortisol resistance in AN. 3) Both undernutrition and abnormal hormone secretion (LEP, F, fT3, IGF-1, LH, E2) are related to social self-withdrawal, defensive attitudes, low self-esteem and high level of self-supervision in AN.
AuthorsMałgorzata Smiarowska
JournalAnnales Academiae Medicae Stetinensis (Ann Acad Med Stetin) Vol. 48 Pg. 351-65 ( 2002) ISSN: 1427-440X [Print] Poland
Vernacular TitleLeptyna i jej potencjalny udział w patomechanizmie niektórych zaburzeń hormonalnych i metabolicznych u chorych z jadłowstretem psychicznym.
PMID14601488 (Publication Type: Clinical Trial, Controlled Clinical Trial, Journal Article)
Chemical References
  • Leptin
  • Human Growth Hormone
  • Insulin-Like Growth Factor I
  • Hydrocortisone
Topics
  • Adipose Tissue (metabolism)
  • Adult
  • Amenorrhea (etiology, metabolism)
  • Anorexia Nervosa (complications, metabolism)
  • Female
  • Human Growth Hormone (metabolism)
  • Humans
  • Hydrocortisone (metabolism)
  • Hypothalamus (metabolism)
  • Insulin Resistance
  • Insulin-Like Growth Factor I (metabolism)
  • Leptin (metabolism)
  • Metabolic Diseases (etiology, metabolism)
  • Nutritional Status
  • Starvation (metabolism)
  • Thyroid Diseases (etiology, metabolism)

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