THE RELATIONSHIP BETWEEN ADIPOSITY AND INSULIN SENSITIVITY IN CAMEROONIAN WOMEN LIVING WITH THE POLYCYSTIC OVARIAN SYNDROME

DOH Emmanuella NAA'JEH MBIENDA (demmanue2001@yahoo.ca)
General Medicine, Faculty of Medicine and Biomedical Sciences; University of Yaounde I
July, 2015
 

Abstract

One of the commonest, heterogeneous, ovulatory disorders among women of reproductive age is the polycystic ovarian syndrome also called the Stein-Leventhal syndrome. Although this condition brings about many unrelated symptoms, obesity and/or overweight remain a very common symptom. Its cause still remains unknown and thus limiting the proper management of this syndrome.
Insulin resistance being a major link to various metabolic diseases such as diabetes mellitus is associated to this condition rendering it a cause of diabetes in young female adults. Several studies have been carried out with the aim of finding the aetiology of this insulin resistance in PCOS. Our study aimed at evaluating the variation of insulin sensitivity in the presence or absence of excessive adipose tissue.
We undertook a cross-sectional, analytical, comparative study on three main groups of women, who had previously given their consent. These groups were made up of 14 PCOS women (subdivided into 6 obese PCOS and 8 non obese PCOS) and 10 non obese non PCOS women. These women underwent anthropometric, percent body fat, fat mass, and lean mass measurements using standard methods. Biological tests such as blood urea nitrogen and serum creatinine were performed on blood samples collected before they underwent the 2 – 3hrs hyperinsulinemic-euglycemic clamp. Calorimetry was performed on another day using a well calibrated calorimeter (ReeVue).
Our results show that obese PCOS women had an android fat distribution based on a greater waist circumference (p= 0.0023) [99 (93 - 104)]cm, fat mass (p=0.0015) [41.2 (30.2 - 47)]kg and a lesser lean mass (p=0.0378) [56.3 (51 – 57.7)]kg when compared to the non obese PCOS women [87 (78 - 93)] and the non obese non PCOS women [77 (69 - 83)]. The non obese PCOS women also had an android fat distribution. The obese PCOS women had a relatively lower insulin sensitivity when compared to the non obese PCOS and the non obese non PCOS women based on the significant differences in the M-value and adjusted M-value for lean mass (p =0.002 and p=0.012 respectively). The obese PCOS women were less sensitive to insulin; [6.6 (5.5 - 7.3)]mg/kg/min and [11.2 (10.1 - 12.4)] mg/kg/min. as compared to the non obese PCOS women [9.1 (7.7 - 10)] and [12.9 (12.1 - 13.8)] based on the M value and adjusted M value for lean mass but the non obese PCOS women where also less insulin sensitive when compared to the non obese non PCOS women [11.9 (9.4 - 14.5)] and [16.6 (13.8 - 17.9)]. There was no significant difference in the median of the resting energy expenditure although it showed a trend.
The obese PCOS women therefore had an android obesity and lower insulin sensitivity hence more likely to be insulin resistant when compared to the non obese PCOS and the non obese non PCOS women but the non obese PCOS women also presented an android obesity and a lower sensitivity to insulin when compared to the non obese non PCOS women and were thus also likely to be insulin resistant.
Our findings suggest that the polycystic ovarian syndrome is associated to insulin resistance even in the absence of obesity. PCOS-associated insulin resistance is further increased by obesity. The distribution of excess adiposity in this syndrome is mainly abdominal resulting in an android fat distribution and obesity does not seem to be explained by the resting energy expenditure but may be due to intake. These findings could have important clinical and therapeutic outcomes.


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