Mani Ravishankar Ram1, Pulliangudi Gokulakrishnan Sundararaman2, Selvi Mahadevan3, Raghunathan Malathi1. 1. Department of Genetics, Dr ALM PG Institute of Basic Medical sciences, University of Madras, Taramani. 2. Department of Endocrinology, Institute of Obstetrics and Gynecology, Egmore, and. 3. Department of Obstetrics and Gynecology, Padma Clinic and Nursing Home, Poonamallee High Road, Chennai, Tamilnadu, India.
Abstract
Background: In polycystic ovary syndrome (PCOS), the leptin (OB protein) is related to reproductive function and inflammatory response. Leptin and cytokines have been thought to be putative local regulators in PCOS. Methods: To examine the relationship between serum leptin and serum interleukin-6 (IL-6), interleukin-8 (IL-8) and tumor necrosis factor-α (TNF-α) levels in underweight, overweight, obese and morbidly obese PCOS and non-PCOS subjects compared with normal weight, regularly menstruating women. Results: Leptin levels are highly correlated with TNF-α, IL-6 and IL-8. There is a significant dependent increase with the degree of obesity, but in underweight PCOS subjects, leptin levels are elevated irrespective of the body mass index. Conclusion: The present study showed that leptin levels were elevated in underweight and morbidly obese PCOS subjects. This could be the result of impaired expression of leptin in PCOS, leading to leptin resistance. As a result of this regulation, TNF-α, IL-6 and IL-8 were also elevated in morbidly obese and underweight PCOS subjects. In obese subjects, where there was an increase in adipose mass, increased levels of leptin were observed and this was attributed to the inflammatory properties while increasing the adipose mass. Serum IL-6 and IL-8 circulate at high levels and are more important systemically. They are, perhaps, the hormonal factors that induce leptin and insulin resistance in underweight PCOS subjects. Therefore, leptin and inflammatory markers were acting at paracrine and endocrine levels in PCOS subjects. (Reprod Med Biol 2005; 4: 247-254).
Background: In polycystic ovary syndrome (PCOS), the leptin (OB protein) is related to reproductive function and inflammatory response. Leptin and cytokines have been thought to be putative local regulators in PCOS. Methods: To examine the relationship between serum leptin and serum interleukin-6 (IL-6), interleukin-8 (IL-8) and tumor necrosis factor-α (TNF-α) levels in underweight, overweight, obese and morbidly obese PCOS and non-PCOS subjects compared with normal weight, regularly menstruating women. Results:Leptin levels are highly correlated with TNF-α, IL-6 and IL-8. There is a significant dependent increase with the degree of obesity, but in underweight PCOS subjects, leptin levels are elevated irrespective of the body mass index. Conclusion: The present study showed that leptin levels were elevated in underweight and morbidly obese PCOS subjects. This could be the result of impaired expression of leptin in PCOS, leading to leptin resistance. As a result of this regulation, TNF-α, IL-6 and IL-8 were also elevated in morbidly obese and underweight PCOS subjects. In obese subjects, where there was an increase in adipose mass, increased levels of leptin were observed and this was attributed to the inflammatory properties while increasing the adipose mass. Serum IL-6 and IL-8 circulate at high levels and are more important systemically. They are, perhaps, the hormonal factors that induce leptin and insulin resistance in underweight PCOS subjects. Therefore, leptin and inflammatory markers were acting at paracrine and endocrine levels in PCOS subjects. (Reprod Med Biol 2005; 4: 247-254).
Entities:
Keywords:
body mass index; cytokine parameters; percentage of body fat; polycystic ovary syndrome; serum leptin
Authors: V Mohamed-Ali; S Goodrick; A Rawesh; D R Katz; J M Miles; J S Yudkin; S Klein; S W Coppack Journal: J Clin Endocrinol Metab Date: 1997-12 Impact factor: 5.958
Authors: R V Considine; M K Sinha; M L Heiman; A Kriauciunas; T W Stephens; M R Nyce; J P Ohannesian; C C Marco; L J McKee; T L Bauer Journal: N Engl J Med Date: 1996-02-01 Impact factor: 91.245