It is known, that sleep-disordered breathing can affect patients with various endocrine diseases. Obstructive, central and mixed
types of sleep apnea syndrome are known to occur in obesity, hypothyroidism, acromegaly, diabetes mellitus, especially with diabetic neuropathy,
Cushing syndrome and polycystic ovary syndrome. The pathogenic mechanisms and pathophysiology of оbstructive sleep apnea
in patients with different endocrine diseases, clinical manifestations and treatment of sleep apnea are reviewed in this article.

The studies of perinatal factors long-term effects on obesity development are summarized in this article. Maternal body mass
and nutrition role during pregnancy was demonstrated in Dutch hunger studies and several works in vivo. The association between birth
weight, obesity, and abdominal fat distribution in future life were demonstrated several times. Breast feeding duration and risk of obesity
have inverse association, but excessive breast feeding also can increase obesity risk. Early accelerated weight gain and further risk of obesity
are also associated. Based on the effect of nitrition in preterm newborns study and several works in vivo it is hypothesized that increased
food consumption during infancy can program elevated leptin concentrations for fat mass ratio durng future life. Further investigations
in this area can lead to breakthrough in solving the problem of obesity and overweight prophylaxis.

Tobacco smoking causes a lot of human deseases and is one of the main reasons of premature death. Smoking cessation is very
important for the patient's health but difficult for them due to development of nicotine dependence. Tobacco dependence is a chronic
disease. Smoking Cessation Clinical Practice Guideline, published in 2008, emphasize the dire health consequences of tobacco dependence,
regulate the way of treating patients who want to quit smoking, recommending the use of effective treatments, including counseling
and medications. Seven first-line medications (5 nicotine and 2 non-nicotine, including Varenicline) that reliably increase long-term
smoking abstinence rates are now available. Smoking cessation is accompanied by a moderate weigh gain. And its a strong motivational
factor to continue smoking, espcially for women. Сounseling, healthy food and physical activity are recommended for such patients.

Review coverts the basic metabolic disorders, characteristic for adult patients with hypopituitarism which frequently cannot be
solved by means of traditional replacement hormonal therapy. Positive influence of rGH therapy has proved necessity of its application
for these patients. Complex replacement of all pituitary deficiencies, including GH, allows an organism to work in the conditions of the
hormonal metabolism as much as possible similar to normal, completely leveling or reducing to a minimum of metabolic consequences
common for adults with hypopituitarism.

There are several pseudogenerics of Meridia® and Xenical®. Lindaxa®, registered in Russia, as a generic of Meridia®, can be at
a disadvantage to a brand on cost-quality ratio.

This article shows a significant efficacy and safety data of original drug Xenical in complex treatment of overweight and obesity
patients. It is emphasized that this data describe properties of original Xenical, but not generics. The generic drug Orsoten has completely
different physicochemical characteristics comparing to Xenical, this differences may lead to increase in allergic reactions and increase of
frequency and intensity of side effects.

The aim of this study was to investigate the effect of acute hyperinsulinemia to fasting leptin level (fL) secretion and leptin
secretion during intravenouse glucose tolerance test (IVGTT). Methods. 32 T2DM women without antidiabetic drugs were studied.
Median age of participants was 57,5[50,0;62,5] years, median body mass index (BMI) was 32,7[29,1;37,1]. Glucose intravenouse
bolus solution (40%) was dosing (0,75 g/kg BM). Insulin level was investigated in fasting state (FI), 2 min, 70 min and 120 min after
glucose loading. Leptin was investigated in fasting (FL) and 120 min after glucose loading. Results. FL level was 21,1[13,6;39,0]
ng/ml. Relationships between FL and HOMA-R, аnd between FL and FI were enough strong (r=0,5, р<0,05). FL in the patient
with moderate diabetes control was twice as much compared to FL in patients with poor diabetes control: (28,0[16,8;47,5] v.s.
12,6[9,2;14,3] ng/ml, (р<0,05)). We found a significant decrease in leptin level at 120 min IVGTT (11% from FL, (р<0,05)). The
most reduction of leptin level was in moderate diabetes control group, which had the overall area under insulin curve. We discovered
a correlation between percentage of leptin reduction and insulin increase on 70 minute of IVGTT (r=0,5, р<0,05). Inverse correlation
was found between percent of leptin reduction in IVGTT and high density lipoprotein level (r=-0,4, р<0,02). Conclusion. FL in
moderate diabetes control group was two times higher compared to poor diabetes control group. Leptin level after glucose loading
was decreased compared with FL.

At present, the epidemic of overweight and obesity is one of the most pressing public health problems worldwide.
Pharmacotherapy is often initiated to increase the effectiveness of obesity therapy, including orlistat, which is a long-acting inhibitor of
gastric and pancreatic lipases that reduces splitting and subsequent absorption of fat food. Till the recent time the only available orlistat
preparation was Xenical (F. Hoffman La Roche Ltd, Switzerland). In 2009, in Russia was registered another trade name of drug - Orsoten
(KRKA, Slovenia), which is the first generic drug orlistat. The article shows the results of a study conducted to examine the clinical
equivalence, efficacy and safety of the drug Orsoten compared with Xenical in obese patients.

We examined 56 normoprolactinemic women of reproductive age (18-45 y.o.) with isolated hypogonadotropic hypogonadism
(group 1) initially and on treatment with 2 mg of 17beta-estradiol and 10 mg of dydrogesterone in sequenced manner (HRT), duration
of HRT was from 18 to 42 (median 36) months; 45 healthy women (20-38 y.o.) were included in control group 2. Initially hypercholesterolemia
was observed in 50% of cases in group 1 and 6.6% in group 2 (z=12,29, p=0,0005); nevertheless, the difference in lipid levels
between groups 1 and 2 was not statistically significant: total cholesterol levels 5,2 (4,3; 6,0) mmol/l and 4,63 (4,15; 5,15) mmol/l respectively
(1vs2, р=0,1); triglycerides 0,8 (0,62; 1,3) mmol/l and 0,76 (0,6; 0,85) mmol/l (1vs2, р=0,08); HDL 1,89 (1,24; 2,1) mmol/l
and 1,79 (1,44; 2,8) mmol/l (1vs2, p=0,85); LDL 2,7 (2,2; 3,2) mmol/l and 2,75 (2,3; 3,3) mmol/l (1vs2, p=0,64). In group 1 decrease
of total cholesterol and triglycerides concentrations was found on HRT: total cholesterol 4,8 (3,95; 5,1) mmol/l (before vs on treatment
p=0,041), triglycerides 0,65 (0,6; 0,9) (before vs on treatment p=0,044) respectively, changes in HDL and LDL levels were not revealed.
Initial concentrations of Ca++, P, and alkaline phosphatase (AP) were within normal range in all women. However, concentrations of
Ca++ and AP were higher in group 1 compared to group 2: Ca++ 1,13 (1,08; 1,19) mmol/l and 1,05 (1,03; 1,09) mmol/l (1vs2,
p=0,0016); AP 161,5 (141,8; 183) IU/l and 141,0 (119; 151) IU/l (1vs2, p=0,044). On HRT reduce in Ca++ and AP concentrations
was observed: Ca++ concentrations 1,05 (1,03; 1,10) mmol/l (before vs on treatment p=0,004), AP 139 (112; 143) IU/l (before vs on
treatment p=0,004). HRT was accompanied by improvement of clinical symptoms, had no influence on thyroid function, and provoked
physiological rise of prolactin levels.Thus, despite lacking the expressed biochemical disorders, isolated hypogonadotropic hypogonadism
in women of reproductive age have hidden negative impact on lipid and mineral metabolism. Long term HRT is safe and significantly
improved parameters of lipid and mineral homeostasis in this cohort of patients.

The reported clinical case represents an example of characteristic traits in lipid metabolism and fat tissue deposition in hypercorticosolism.
Probable causes for fat mass expansion in glucocorticosteroid excess, its distinctive cushingoid distribution, role of
11β-HSD1 and glucocorticoid receptors and reversibility of specific abnormalities after correction of hypercortisolism are discussed in
the context of physiological and pathological aspects of glucocorticosteroid action.