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polycystic ovarian syndrome ( pcos ) is one of the most common endocrine disorders among women of the reproductive age
. it is commonly undiagnosed due to the fact that its symptoms are heterogeneous and seem to have no relation with each other .
obesity is a common symptom of polycystic ovarian syndrome although its cause still remains unknown .
in some recent studies , evidence has brought forth a relationship between some types of obesity and an alteration in insulin sensitivity .
android obesity is the most indexed in this alteration and this is the main type present in women living with pcos [ 4 , 5 ] .
this alteration in insulin sensitivity is also an associated and common factor in the polycystic ovarian syndrome .
several mechanisms though not well understood have been incriminated in the insulin resistance associated with pcos with obesity as the leading cause .
also a decrease in insulin receptor autophosphorylation and tyrosine phosphorylation of insulin receptor substrate-2 induces impairment of the insulin signal pathway hence increasing insulin resistance [ 7 , 8 ] .
central obesity is thought to be strongly involved in insulin resistance in these women but is the obesity the cause of this insulin resistance ? if no , the insulin resistance may be independent of the obesity and directly related to the pathogenesis of pcos which will require further investigation .
this knowledge may reveal novel therapeutic targets for the management of this pathology which has a devastating effect on a woman 's self - esteem due to its aesthetic , reproductive , and cultural manifestations in our african setting .
several studies have been carried out worldwide in order to better understand insulin resistance in pcos subjects using gold standard methods such as the euglycemic - hyperinsulinemic clamp . to the best of our knowledge
, we carried out this study to investigate the relationship between obesity and insulin sensitivity in cameroonian women living with pcos .
we hypothesized that obesity and pcos both independently and synergistically cause insulin resistance in cameroonian women living with pcos .
we carried out a cross - sectional , comparative study at the endocrinology and metabolic disease unit of the yaound central hospital , yaound ( cameroon ) .
we enrolled 24 women of reproductive age ( 1845 years ) among which were obese pcos patients ( n = 6 ) , nonobese pcos patients ( n = 8) , and healthy adults ( n = 10 ) . diagnosis of pcos was confirmed according to clinical presentation , presence of multiple cysts in the ovaries during ultrasonography , and serum hormonal imbalance ( elevated levels of testosterone and lh ; low progesterone and estrogen levels ; and normal fsh levels ) in accordance with the rotterdam criteria .
women with amenorrhea ( cycle interval  6 months ) and/or midluteal progesterone level 15  nmol / l were considered anovulatory .
normal range was 2.510.2  u / l for fsh and 1.912.5  u / l for lh .
hirsutism was assessed by the modified ferriman - gallwey score , the gold standard for clinical evaluation of hirsutism , with a cut - off level of 8 .
obesity was determined based on the who classification of adult underweight , overweight , and obesity according to bmi .
pregnancy , breast feeding , intercurrent illness , the use of any medication that could affect insulin metabolism , smoking , recent infection less than ten days prior to inclusion , and creatinine clearance 60  ml / min/1.73  m were exclusion criteria .
the study protocol was approved by the institutional research ethical committee of the faculty of medicine and biomedical sciences , yaound , and by the institutional review board of the yaound central hospital .
clinical and anthropometric data were collected using a predesigned questionnaire before body composition analysis and functional tests .
insulin sensitivity was assessed using a 2-hour euglycemic - hyperinsulinemic clamp at 80  mu / m / min .
it consisted of using an impedance meter ( tanita , tanita corporation , 1 - 14 - 2 maeno - cho , tabashi - ku , tokyo , japan ) .
this noninvasive test simply involves the placement of two electrodes under the person 's feet and two electrodes in their hands . a low level
the output variables include the percent of body fat , fat mass , fat - free mass , and bone mass .
salt lake city , ut 84120 , usa ) was performed after a fast of at least 3  hrs .
participants were required not to smoke , drink alcoholic beverages , or do sports 24  hrs prior to the exploration .
they were installed in a supine position and rested 20  mins in the said position .
after an overnight fast , participants were admitted into the clinical research facility of the endocrine unit of yaound central hospital .
rapid insulin ( actrapid hm novo nordisk a / s , 2880 bagsvaerd , denmark ) concentrated at 100  mu / ml installed in a syringe pump ( alaris medical systems uk ltd . , basingstoke rg22 4bs , uk ) and 10% dextrose solution were infused via the right antecubital vein .
a priming dose of insulin was given over the first 10 minutes followed by a constant infusion rate of 80  mu / m / min up to the 120th minute [ 12 , 13 ] .
the 10% dextrose solution was infused as from the 11th minute at variable rates modifiable every 5 minutes using an infusion pump ( ivac corporation , model 598 , san diego , california ) with the aim of maintaining capillary blood sugar levels at 5.5  0.5  mmol / l .
capillary blood sugar measurements were done with a glucometer and strips ( onetouch ultra 2 , lifescan europe , division of cilag gmbh international , 6300 zug , switzerland ) .
blood samples were collected at baseline and the 100th , 110th , and 120th  min .
insulin sensitivity was calculated when the coefficient of variations of glycaemia and insulinemia and the rate of glucose infusion were less than 5% by the m value ( mg / min / kg ) which represents glucose disposal rate during insulin infusion .
m value was calculated as the rate of glucose infusion minus the space of correction ( sc ) of glucose and then was adjusted for lean body mass . during the last 20 minutes of the euglycemic - hyperinsulinemic clamp , glycaemia is not constant , and sc has been defined to adjust for variations in glucose infusion rate and glycemic levels .
sc was calculated using difference of glucose levels at the beginning and the end of the steady state period multiplied by 0.095 .
the entered data was then extracted to stata 12.0 ( statacorp , college station , tx , usa ) for analysis .
qualitative variables were presented as a count and percentage while continuous variables as median [ interquartile range ] .
medians were compared between groups by the kruskal - wallis and the mann whitney - wilcoxon rank sum test . the threshold for significance
the median [ interquartile range ] age of the individual groups of our study was 26 [ 2330 ] years for obese pcos patients , 27 [ 2429 ] years for nonobese pcos patients , and 23 [ 23 - 24 ] years for healthy subjects . 

bmi was significantly higher in obese pcos subjects than in the nonobese subjects who were higher than the heathy subjects ( p = 0.0003 ) . also , the median fat mass ( p = 0.0015 ) and lean mass ( p = 0.0378 ) were significantly higher in obese pcos subjects than in nonobese pcos subjects which were equally higher than in healthy subjects .
other parameters significantly higher in obese pcos subjects were waist circumference and body fat percentage .
our study populations had similar fasting plasma glucose and systolic and diastolic blood pressure . 

a greater percentage of obese pcos subjects eat fewer vegetables and more fruits than nonobese pcos subjects and controls .
they are also more involved in sporting activities . following the euglycemic - hyperinsulinemic clamp , the clamp - derived m value adjusted for lean body mass expressed in mg / kg / min was lower in nonobese pcos subjects when compared to healthy subjects and even lower in obese pcos subjects ; p = 0.012 ( table 3 ) .
indirect calorimetry measurements of resting energy expenditure were highest in obese pcos subjects followed by nonobese pcos subjects and lowest in healthy subjects but were not significant ; p = 0.306 ( figure 1 ) . 
 table 4 shows the correlation between clinical parameters , biological characteristics , and the m value adjusted for lean body mass expressed in mg / kg / min in our study population . among all the parameters , body mass index was inversely correlated with lean body mass adjusted m value ( r = 0.56 ; p = 0.005 ) . 

figure 2 shows the regression between the lean body mass adjusted m value and the bmi of our study population ( r = 0.31 , p = 0.0048 ) .
this study evaluated the variation in insulin sensitivity in women living with polycystic ovarian syndrome in relation to obesity . in our study , m value and m adjusted to lean mass were lower in both obese and nonobese people living with pcos .
these findings are similar to those found in study populations of various ethnic groups using the euglycemic - hyperinsulinemic clamp technic .
they found that in their populations women with pcos were more insulin resistant even when matched for bmi with controls .
furthermore , they showed that body fat contributes to determining insulin resistance in these subjects [ 14 , 15 ] .
the fact that both obese and nonobese women living with pcos were less insulin sensitive than their controls shows that although obesity may play a role in insulin resistance seen in this syndrome , there are other factors associated with pcos implicated .
insulin potentiates steroidogenic response to gonadotrophins both in vivo and in vitro ; hence , during hyperinsulinemia there will be elevated androgen levels .
insulin also increases the number of lh receptors in granulosa cells and in concert with fsh increases lh - binding capacity and is one reason for the elevated lh seen in pcos .
this elevated lh on its own increases androgen levels via its involvement in androstenedione production .
insulin response to an oral glucose load is higher in lean and obese pcos women compared to healthy ones .
this clearly signifies that , irrespective of the presence or absence of obesity , insulin resistance is associated with pcos . the lower insulin sensitivity in obese pcos
women compared to nonobese pcos women shows that though obesity may not be the only cause of insulin resistance in pcos subjects , it worsens the insulin resistance in pcos   and therefore should be a treatment goal .
effectively , it has been shown that weight loss in obese pcos subjects even without other therapeutic agents can restore insulin sensitivity .
body composition analysis in this study revealed that pcos was associated with android obesity as shown by a disproportionally high waist circumference for a given bmi .
this type of fat distribution was similarly found in caucasian women even in nonobese pcos women . abdominal obesity or central obesity
race also plays an important role in severity of adipose tissue distribution as africans are more prone to subcutaneous adiposity than caucasians [ 21 , 22 ] .
we can conclude that though android obesity may not be the sole determinant of insulin resistance in pcos it is an important one .
our results showed no significant difference in the resting energy expenditure ( ree ) of the three groups .
similar results were obtained in another study where there was no difference in ree between pcos subjects and controls even after adjusting for age and bmi . however ,
these results are in contrast to those from other studies which showed that pcos is associated with decreased ree and postprandial thermogenesis as a result of insulin resistance [ 24 , 25 ] .
this was probably due to our small sample size in comparison to the large study population in those studies .
in addition , our population had a higher bmi than in the above - mentioned studies and this may explain the tendency for ree to increase among the pcos women in our study .
it is useful to report the trend though because it suggests that the etiology of obesity is not due to ree although more studies should be performed on a larger cohort before drawing firm conclusions .
the lack of a difference between the groups suggests that poor lifestyle habits ( such as diet and inactivity ) may remain the main predisposing factor of the obesity in pcos women .
this means that dietary intervention and increased physical activity can significantly help to improve insulin sensitivity and obesity in women living with pcos .
we studied body composition , clamp - derived insulin sensitivity , and resting energy expenditure in obese and nonobese pcos sub - saharan women .
insulin sensitivity was decreased in nonobese pcos women and further decreased in the presence of obesity without a clear relation with resting energy expenditure .
objectives . we aimed to assess the variation of insulin sensitivity in relation to obesity in women living with pcos in a sub - sahara african setting . methods . 
 we studied body composition , insulin sensitivity , and resting energy expenditure in 14 pcos patients ( 6 obese and 8 nonobese ) compared to 10 matched nonobese non - pcos subjects . 
 insulin sensitivity was assessed using the gold standard 80  mu / m2/min euglycemic - hyperinsulinemic clamp and resting energy expenditure was measured by indirect calorimetry . 
 results . 
 insulin sensitivity adjusted to lean mass was lowest in obese pcos subjects and highest in healthy subjects ( 11.2 [ 10.112.4 ] versus 12.9 [ 12.113.8 ] versus 16.6 [ 13.817.9 ] , p = 0.012 ) ; there was a tendency for resting energy expenditure adjusted for total body mass to decrease across the groups highest in obese pcos subjects ( 1411 [ 13681613 ] versus 1274 [ 11741355 ] versus 1239 [ 11951454 ] , p = 0.306 ) . conclusion . in this sub - saharan population , 
 insulin resistance is associated with pcos per se but is further aggravated by obesity . 
 obesity did not seem to be explained by low resting energy expenditure suggesting that dietary intake may be a determinant of the obesity in this context .