A comprehensive assessment of metabolic parameters in obese patients on xenical
- Authors: Ametov AS1, Demidova TY.1, Tselikovskaya AL1
-
Affiliations:
- РМАПО
- Issue: Vol 79, No 1 (2004)
- Pages: 49-53
- Section: Editorial
- URL: https://bakhtiniada.ru/0040-3660/article/view/29764
- ID: 29764
Cite item
Full Text
Abstract
Material and methods. The study included 60 patients with body mass index (BMI) over 30 kg/m2, mild and moderate arterial hypertension, dyslipidemia, impaired glucose tolerance (IGT) and diabetes mellitus (DM) type 2. The patients were divided into two groups. 30 patients of group 1 received xenicaf® in a dose 120 mg 3 times a day for 24 weeks. 30 patients of the control group received only the above diet for 24 weeks. The examination included 24-h monitoring of arterial pressure, anthropometric measurements, tests for glycemia, C-peptide, cholesterol, triglycerides (TG), LDLP, HDLP. Results. Group 1 patients reduced their weight by 10.8 + 7.5 kg and fat tissue mass by 9.4 ± 9.2 kg. This was in correlation with improvement of fatty, carbohydrate metabolism, arterial pressure. After 24 weeks of therapy xenical lowered cholesterol by 15%, LDLP cholesterol by 20%, TG by 28%, systolic and diastolic pressure by 5 and 4%.
Conclusion. Combination ofxenical with hypocaloric diet can be used in therapy of patients with metabolic syndrome.
Keywords
About the authors
A S Ametov
РМАПОМосква; РМАПО
T Yu Demidova
РМАПОМосква; РМАПО
A L Tselikovskaya
РМАПОМосква; РМАПО
References
- Аметов А. С., Демидова Т. Ю., Целиковская А. Я. Ожирение и сердечно-сосудистые заболевания. Тер. арх. 2001; 66-69.
- Аметов А. С., Демидова Т. Ю., Пархонина Е. С. Ожирение - основа метаболического синдрома. Лечащий врач 2001; 5: 28-32.
- Бутрова С. А. Метаболический синдром: патогенез, клиника, диагностика, подходы к лечению. Рус. мед. журн. 2000; 9: 56-60.
- Hodge A. M., Boyko E. J., de Courten M. et al. Leptin and other components of the Metabolic Syndrome in Mauritius-a factor analysis. Int. J. Obes. Relat. Metab. Disord. 2001; 25 (suppi. 1): 126-131/
- Sorensen T. I., Echwald S., Holm J. С. Leptin in obesity. Br. Med. J. 1996; 313: 953-954/
- Аметов А. С., Демидова Т. Ю., Целиковская А. Л. Влияние лептина на регуляцию массы тела. Сердечная недостаточность. 2001; 3: 135-137.
- Reaven G. M. Insulin resistance and hyperinsulinemia in individuals with small, dense, low density particles. J. Clin. Invest. 1993; 92: 141-146.
- Reaven G. M. Insulin resistance, compensatory hyperinsulinemia, and coronary heart disease. Diabetologia 1994; 37: 948- 952.
- Arvaniti K., Ricquier D., Champigny O., Richard D. Leptin and corticosterone have opposite effects on food intake and the expression of UCP1 mRNA in brown adipose tissue of lep(ob)/ lep(ob) mice. Endocrinology 1998; 139 (suppl. 9): 4000-4003.
- Bryson J. M. The future of leptin and leptin analogues in the treatment of obesity. Diabet. Obes. Metab. 2000; 2 (suppl. 2): 83-89.
- Cam J. F., Kolaczynski J. W. Leptin: the tale of an obesity gene. Diabetes 1996; 45: 1455-1462.
- Hotamisgilil С. S., Arner P., Caro J. F. et al. Increased adipose tissue expression of tumor necrosis factor in a human obesity and insulin resistance. J. Clin. Invest. 1995; 95: 1409-1415.
- Hotamisgilil С. S., Shargill N. S., Spiegelman В. М. Adipose expression of tumor necrosis factor-a: direct role in obesitylinked insulin resistance. Science 1993; 259: 87-91.
- Soma S. C., Yamamoto M. T. et al. BRL 49653 blocks the lipolytic actions of tumor necrosis factor-a: a potential new insulin-sensitizing mechanism for thiazolidinediones. Diabetes 1998; 47: 691-695.
- Goldstein D. J. Beneficial health effects of modest weight loss. Int. J. Obesity 1992; 16: 397-415.
- Lean M. E., Han T. S. Impairment of health and quality of life in people with large waist circumference. Lancet 1998; 351: 853-856.
- Зимин Ю. В. Происхождение, диагностическая концепция и клиническое значение синдрома инсулинорезистентности или метаболического синдрома X. Кардиология 1998; 6: 71-81.
Supplementary files
