Effect of treatment with metformin on omentin-1, ghrelin and other biochemical, clinical features in PCOS Patients.
Polycystic ovary syndrome (PCOS) is a common endocrine metabolic disease which occurs in 5-10% of reproductive age women. (1-3) PCOS is an inherited disease affecting women of childbearing age. (4) The disorder causes multiple abnormal cysts and enlarged ovaries, so that they do not produce the normal number of eggs and do not ovulate normally. The disease is present at birth but is not cause symptomatic until a genetic component and clinical feature of this disorder change throughout the life span, starting from adolescence to postmenopausal age. Hence, no effort has been made to define the differences in the phenotype and clinical presentation according to age. (5,6)
The course of treatment for women with PCOS largely depends on the severity of an individual's symptoms. Well-defined published data indicate a high risk for the development of Type 2 diabetes mellitus (T2DM) and Cardiovascular Disease (CVD) in women with PCOS. In view of the lack of protective effect of female sex on CVD risk in patients with diabetes, the associated risks of CVD are magnified in women with diabetes who have PCOS. (7,8) Clearly, this situation means that PCOS is a general health disorder for young women, with potential for reversal of some of the associated risk with early diagnosis and treatment. (9) Lifestyle modification with weight loss and exercise, avoidance of tobacco, correction of lipid abnormalities, and use of metformin may be of value. Metformin therapy does not only reduce hyperinsulinism and improve steroidogenic dysfunction, but also it is helpful in achieving better regularity of menses and fertility potential. (10,11) Thiazolidinediones have also been shown to decrease androgen levels, improve ovulation, and reduce progression to overt T2DM in patients with PCOS and impaired glucose tolerance (IGT). (12-14)
Metformin (N, N-dimethylimidodicarbonimidic diamide) is now thought to be of therapeutic value directly and/or indirectly in the management of PCOS. (15) It is the first-line drug of choice for the treatment of T2DM, particularly in overweight and obese people and those with abnormal kidney function.
Ghrelin is a 28 amino acid peptide hormone, which is primarily produced by the stomach, (Fig. 1). (16) Ghrelin has an octanoyl group on the serine at the third position in the amino acid chain which gives the peptide hormone its biological activity. (17)
[FIGURE 1 OMITTED]
Data on ghrelin levels in women with PCOS are rather conflicting; both decreased, (18-20) and elevated, (21) concentrations have been reported, while others have found no significant differences between women with the syndrome and normal ovulatory women. (22) Omentin-1 is a new type of Ca2+-dependent lectin with affinity for galacto furanosyl residues (the last are constituents of pathogens and dominant inmunogens). (23) It is suggested, therefore, that a biological function of omentin-1 is the specific recognition of pathogens and bacterial components, an important role in the innate immune response to parasite infection. (24) A study has been shown that omentin-1 is decreased in patients with PCOS. (25) Glucose and insulin negatively regulate Omentin-1 levels ex-vivo and in vivo.25 Therefore, omentin-1 levels may be predictive of the metabolic consequences or co-morbidities associated with obesity.
After overnight fasting, venous blood samples were aspirated at 08:00-10:00 am during the third and sixth days of the menstrual cycle (early follicular phase) for those of normal cycle. For patients withan ovulation or oligomenorrhea, blood samples were collected regardless of the duration of the cycle. The samples were transferred into clean plain tubes and centrifuged within 30 minutes of collection, then serum from all blood samples were separated, sugar, lipid profile levels were measured using the enzyme colorimetric methods, the rest was stored at -18 [degrees]C until the time of assay.
60 infertile Iraqi women aged 18-37 years (M [+ or -] SD: 26.45 [+ or -] 4.65) were studied. The medical history was taken, body weight and height were measured and body mass index (BMI) was calculated [mean BMI (34.01 [+ or -] 3.54 Kg/[m.sup.2])]. PCOS patients had been already diagnosed and the diagnosis had been confirmed according to the European society of human reproduction and embryology and American society for reproductive medicine criteria. PCOS is diagnosed if there are any two of the following; a) presence of polycystic ovary on ultrasound examination, b) clinical or biochemical hyperandrogenemia, and c) menstrual dysfunction with an ovulation.
The 60 PCOS women were re-evaluated after three months of treatment with 850 mg metformin twice daily. Body Mass Index (BMI) was calculated as kg/[m.sup.2] and waist-to-hip ratio (WHR) was determined in all the subjects. Omentin-1, ghrelin and insulin hormones were determined by ELISA methods. Serum fasting glucose and lipid profile levels were measured by enzymatic method supplied by Giesse Diagnostic.
The homeostasis model assessment (HOMA) was used to calculate an index of insulin resistance for each patient, and beta-cell function was estimated from fasting insulin and glucose levels by the homeostasis model assessment (HOMA-[beta]) using fasting glucose in mmol/L and insulin in [micro]IU/ml, the index for insulin resistance, HOMA IR, was defined as (insulin x glucose) /22.5 and HOMA [beta]-cell function x 20 x insulin/(glucose-3.5). (26)
All statistical analysis in t h e study was performed using SPSS version 15.0 for Windows (Statistical Package for Social Science, Inc., Chicago, IL, USA). Descriptive analysis was used to show the mean and standard deviation of variables. The significance of differences between mean values was estimated by Student t-test. The probability p<0.05 was considered statistically significant, while p>0.05 was considered statistically insignificant. Correlation analysis was used to test the linear relationship between t h e parameters. ANOVA test was used to show the differences between variables of different groups.
In a PCOS subjects treated with metformin, the mean BMI and WHR had significantly decreased (p<0.005) and (p<0.01) respectively after 3 months as shown in Table 1. Serum levels of HDL-cholesterol were increased and the total cholesterol/HDL-cholesterol ratio was significantly decreased, (p<0.05) after three months of treatment. Serum concentrations of insulin, HOMA and HOMA [beta]-cell % were significantly decreased (p< 0.05), (p< 0.01) and (p<0.05) respectively after three months of treatment. In PCOS women treated with metformin for three months, serum ghrelin levels significantly increased (p<0.01) as shown in Table 1.
Serum levels of omentin1 were significantly increased (p<0.05) after three months of treatment, (Table 1). It is to best of the authors' knowledge that the effects of treatment on serum omentin1 level in the present study are shown for the first time. In the present study, the effects of metformin on several parameters that depend on the omentin1 ratios were observed. (Table 2)
Omentin-1(ng/ml) was negatively correlated with BMI (r=-0.435, p<0.001), insulin (r=-0.424, p<0.001), HOMA (r=-0.415, p<0.001), HOMA [beta]-cell% (r=-0.358, p<0.05), and LDL-cholesterol (r=-0.590, p<0.05) in patients, while no significant correlation was found between omentin-1 and these factors in t h e controls. A significant positive correlation was found between omentin-1 (ng/ml) and QUICKI (r=0.497, p<0.001), and ghrelin (r= 0.511, p<0.001). (Table 3)
Table 4 shows a significant negative correlation between ghrelin (pg/ml) with BMI (r=-0.665, p<0.001), insulin (r=-0.897, p<0.001), HOMA (r=-0.871, p<0.001), HOMA [beta]-cell% (r=-0.683, p<0.001), cholesterol (r=-0.641, p<0.01), TG (r=-0.443, p<0.01), LDL-cholesterol (r=-0.656, p<0.01), LDL:HDL ratio (r=-0.643,p<0.01), and Cholesterol/HDL ratio (r=-0.638, p<0.01) in patients, while no significant correlation was found in these factors in the control group.
A significant positive correlation was found between ghrelin (pg/ml) and QUICKI (r=0.851, p<0.001). (Table 4)
In line with the study results, a dose-response effect of metformin was noticed more than 10 years ago, when it became available in the USA, and since then, the metformin dosage has been increased, with better outcomes. (27)
The present results are in line with those of previous studies on PCOS, where metformin has been shown to improve the lipid profile, mainly by increasing serum HDL-cholesterol concentrations. (28,29) On the other hand, some other studies have shown only a negligible or no effect on lipids in women with PCOS. (30,31) The mechanisms by which metformin improves the lipid profile are not clear.
Metformin has been suggested to reduce lipid uptake or synthesis in the intestine and in the hepatocytes. (32) As observed in previous studies, the improvement of obesity, especially abdominal obesity, with a subsequent decreased release of free fatty acids (FFA) from adipose tissue observed during metformin therapy could also partly explain the improvement of lipid profile during metformin treatment, at least in obese women. (33)
Serum concentrations of insulin, HOMA and HOMA [beta]-cell% were decreased significantly (p<0.05), (p<0.01), (p<0.05) respectively after three months of treatment, (Table 1). The authors suggest that the reduction in hyperinsulinemia observed may be due to improvements in hepatic extraction and insulin sensitivity during therapy with metformin. They also found that metformin reduced basal levels of FFA, which as mentioned above, have a role in reducing glucose disposal in skeletal muscle, leading to impaired insulin sensitivity. Because the waist-to-hip ratio of the patients decreased after therapy, they concluded that the reduction in IR induced by metformin was secondary to its effects on adipose tissue. (34) Two original papers investigating the effect of metformin on IR in women with PCOS reported negative results. (35) The reasons for the partly conflicting results are not clear. A possible explanation is that only around 50% of women with PCOS respond to metformin and this could be why some studies did not report benefits from metformin therapy.
In PCOS women treated with metformin for three months, serum ghrelin levels significantly increased. Moghetti et al. in 2000, found that insulin-resistant PCOS patients treated with metformin showed improved insulin sensitivity in PCOS patients and increased serum ghrelin levels.28 This suggests a link between insulin sensitivity and ghrelin concentrations and shows that the dysregulated ghrelin system in insulin-resistant PCOS women could be normalized by metformin therapy.
Increased in omentin1 level after treatment with metformin may be due to the negative correlation between omentin 1 plasma levels with HOMA, BMI and insulin. These data suggests that some aspect of obesity negatively regulates omentin expression and release into the circulation. In the current study, treatment with metformin significantly decreased both insulin and BMI, so the increase in omentin1 level may be as a result of it. Obesity itself which may contribute in the regulation of the role of omentin in human physiology. (36-38) Consequently, weight loss could be a modulator of omentin expression and function. No previous studies have showed these results. A more detailed research to study the effect of metformin on other cytokines and connection with omentin1 should be conducted.
The results from this study showed a significant increase in omentin1: insulin ratio, omentin1: HOMA ratio and omentin1; HOMA [beta]-cell% ratio. These results in the present study are shown for the first time to the best of our knowledge, thus suggesting that these factors may be useful in following improvements in insulin sensitivity in subjects with PCOS or obesity treated with insulin sensitizers.
However, further studies are needed to validate this measure in other populations with this treatment or with other insulin sensitizers or in patients treated with diet and exercise.
The authors reported no conflict of interest and no funding was received on this work.
(1.) Orio F, Palomba S, Cascella T, Simone B, Biase S, Russo T, et al. Early impairment of endothelial structure and function in young normal-weight women with polycystic ovary syndrome. J Clin Endocrinol Metab 2004; 89(9):4588-4593.
(2.) Trivax B, Azziz R. Diagnosis of Polycystic Ovary Syndrome. Clinical Obstetrics& Gynecology 2007; 50(1):168-177.
(3.) Lobo R, Carmina E. The importance of diagnosing the Polycyctic overy syndrome. Ann Intern Med 2000; 132(12):989-993.
(4.) Janet M, Cassio L, Richard M. Polycystic Ovary Syndrome. JAMA 2007; 297:524.
(5.) Hamzeh R, Balen A. Up-to-date Definition of the Polycystic Ovary and Polycystic Ovary Syndrome. Ultrasound 2006; 14(3):142-144.
(6.) Pascuali R, G ambineri A. Polycystic Ovary Syndrome: A Multifaceted Disease from Adolescence to Adult Age. Ann NY Acad Sci 2006; 1092(1):158-174.
(7.) Gu K, Cowie C, Harris M. Diabetes and decline in heart disease mortality in US adults JAMA 1999; 281(12):1291-1297.
(8.) Mak K, Haffner S. Diabetes abolishes the gender gap in coronary heart disease. Eur Heart J 2003; 24(15):1385-1386.
(9.) Nestler J. Polycystic ovarian syndrome: metabolic and cardiovascular complications. In: Kreisberg RA, program director. Clinical Endocrinology Update 2003 Syllabus. Chevy Chase, MD: The Endocrine Society Press 2003; 299-303.
(10.) Nestler J, Jakubowicz D. Lean women with polycystic ovary syndrome respond to insulin reduction with decreases in ovarian P450c17 a activity and serum androgens. J Clin Endocrinol Metab 1997; 82(12):4075-4079.
(11.) Nestler J, Stovall D, Akhter N, Iuorno M, Jakubowicz D. Strategies for the use of insulin-sensitizing drugs to treat infertility in women with polycystic ovary syndrome. Fertil Steril 2002; 77(2):209-215.
(12.) Belli SH, Graffigna M, Oneto A, Otero P, Schurman L, Levalle O. Effect of rosiglitazone on insulin resistance, growth factors, and reproductive disturbances in women with polycystic ovary syndrome. Fertil Steril 2004; 81(3):624-629.
(13.) Baillargeon J, Jakubowicz D, Iuorno M, Jakubowicz S, Nestler J. Effects of metformin and rosiglitazone, alone and in combination, in nonobese women with polycystic ovary syndrome and normal indices of insulin sensitivity. Fertil Steril 2004; 82(4):893-902.
(14.) Dronavalli S, Ehrmann D. Pharmacologic therapy of polycystic ovary syndrome. Clinical Obstetrics and Gynecology 2007; 50(1):1: 244-254.
(15.) National Institute for Health and Clinical Excellence. Clinical guideline 66: Diabetes--type 2 (update). London, 2000.
(16.) Kojima M, Hosoda H, Date Y, Nakazato M, Matsuo H, Kangawa K. Ghrelin is a growth-hormone-releasing acylated peptide from stomach. Nature 1999; 402(6762):656-660.
(17.) Rosicka M, Krsek M, Jarkovska Z, Marek J, Schreiber V. Ghrelin--a New Endogenous Growth Hormone Secretagogue. Physiol Res 2002; 51(15):435-441.
(18.) Pagotto U, Gambineri A, Vicennati V, Heiman M, Tschop M, Pasquali R. Plasma ghrelin, obesity, and the polycystic ovary syndrome, correlation with insulin resistance and androgen levels. J Clin Endocrinol Metab 2002; 87(12):5625-5629.
(19.) Schofl C, Horn R, Schill T, Schlosser H, Muller M, Brabant G. Circulating ghrelin levels in patients with polycystic ovary syndrome. J Clin Endocrinol Metab 2002; 87(10):4607-4610.
(20.) Moran L, Noakes M, Clifton P, Wittert G, Tomlinson L, Galletly C, et al. Ghrelin and measures of satiety are altered in polycystic ovary syndrome but not differentially affected by diet composition. J Clin Endocrinol Metab 2004; 89(7):3337-3344.
(21.) Wasko R, Komarowska H, Warenik-Szymankiewicz A, Sowinski J. Elevated ghrelin plasma levels in patients with polycystic ovary syndrome. Horm Metab Res 2004 ; 36(3):170-173.
(22.) Orio F, Lucidi P, Palomba S, Tauchmanova L, Cascella T, Russo T, et al. Circulating ghrelin concentrations in the polycystic ovary syndrome. J Clin Endocrinol Metab 2003; 88(2):942-945.
(23.) Schaffler A. Genomic structure of human omentin, a new adipocytokine expressed in omental adipose tissue. Biochim Biophys Acta 2005; 1732(1-3):96-102.
(24.) Gerwick L. Gene transcript changes in individual rainbow trout livers following an inflammatory stimulus, Fish Shellfish Immunol 2007; 22(3):157-171
(25.) Tan B, Adya R, Farhatullah S, Lewandowski C, O'Hare P, Lehnert H, et al. Omentin-1, a Novel Adipokine, is decreased in Overweight Insulin Resistant Women with the Polycystic Ovary Syndrome: ex vivo and in vivo Regulation of Omentin-1 by Insulin and Glucose. Diabetes 2008; 57(4):801-808.
(26.) Ehrmann D, Liljenquist D, Kasza R, Azziz R, Legro R, Mahmoud N. Prevalence and Predictors of the Metabolic Syndrome in Women with Polycystic Ovary Syndrome. J Clin Endocrinol Metab 2006; 91(1):48-53.
(27.) DeFronzo R, Goodman A. Efficacy of metformin in patients with non-insulin-dependent diabetes mellitus--The Multicenter Metformin Study Group. N Engl J Med 1995; 333(9):541-549.
(28.) Moghetti P, Castello R, Negri C, Tosi F, Perrone F, Caputo M, et al. Metformin effects on clinical features, endocrine and metabolic profiles, and insulin sensitivity in polycystic ovary syndrome: a randomized, double-blind, placebo-controlled 6-month trial, followed by open, long-term clinical evaluation. J Clin Endocrinol Metab 2000; 85(1):139-146.
(29.) Fleming R, Hopkinson Z, Wallace A, Green IA, Sattar N. Ovarian function and metabolic factors in women with oligomenorrhea treated with metformin in a randomized double blind placebo-controlled trial. Clin Endocrinol Metab 2002; 87(2):569-574.
(30.) Velazquez E, Mendoza S, Hamer T, Sosa F, Glueck C. Metformin therapy in polycystic ovary syndrome reduces hyperinsulinemia, insulin resistance, hyperandrogenemia, and systolic blood pressure, while facilitating normal menses and pregnancy. Metabolism 1994; 43(5):647-654.
(31.) Ehrmann D, Cavaghan M, Imperial J, Sturis J, Rosenfield R, Polonsky K. Effects of metformin on insulin secretion, insulin action, and ovarian steroidogenesis in women with polycystic ovary syndrome. J Clin Endocrinol Metab 1997; 82(2):524-530.
(32.) Carlsen S, Rossvoll O, Bjerve K, Folling I. Metformin improves blood lipid pattern in nondiabetic patients with coronary heart disease. J Intern Med 1996; 239(3): 227-233.
(33.) Morin L, Vauhkonen I, Koivunen R, Ruokonen A, Martikainen H, Tapanainen J. Metformin versus ethinyl estradiol-cyproterone acetate in the treatment of nonobese women with polycystic ovary syndrome: a randomized study. J. Clin. Endocrinol. Metab 2003; 88(1):148-156.
(34.) De Leo V, la Marca A, Petraglia F. Insulin-lowering agents in the management of polycystic ovary syndrome. Endocr Rev 2003; 24(5):633-667.
(35.) Acbay O, Gundogdu S. Can metformin reduce insulin resistance in polycystic ovary syndrome? Fertil Steril 1996; 65(5):946-949.
(36.) Heilbronn L, Noakes M, Clifton P. Energy restriction and weight loss on very-low-fat diets reduce C-reactive protein concentrations in obese, healthy women. Arterioscler Thromb Vasc Biol 2001; 21(6):968-970.
(37.) Weisberg S, McCann D, Desai M, Rosenbaum M, Leibel R, Ferrante A. Obesity is associated with macrophage accumulation in adipose tissue. J Clin Invest 2003;112(12):1796-808.
(38.) Ryan A, Nicklas B. Reductions in plasma cytokine levels with weight loss improve insulin sensitivity in overweight and obese postmenopausal women. Diabetes Care 2004; 27(7):1699-1705.
From the Department of Acceptable Analysis, Health and Medical Technical College.
Received: 14 Jul 2010
Accepted: 11 Aug 2010
Address correspondence and reprint request to: Dr. Atheer Awad Mehdi, Department of Acceptable Analysis, Health and Medical Technical College, Baghdad, Iraq.
Table 1: The effects of metformin in PCOS patients on clinical and metabolic parameters and on concentrations of lipid profile, ghrelin and omentin1. Characteristic 0 months [n=60] BMI [Kg/[m.sup.2]] Mean [+ or -] SD 33.14 [+ or -] 1.88 WHR Mean [+ or -] SD 0.86 [+ or -] 0.02 Fasting insulin [[micro]u/ml] Mean [+ or -] 20.93 [+ or -] 8.38 SD Fasting blood glucose [mg/dl] Mean [+ or -] 86.60 [+ or -] 7.00 SD HOMA Mean [+ or -] SD 4.61 [+ or -] 2.06 HOMA [beta]-cell % Mean [+ or -] SD 375.90 [+ or -] 194.70 QUICKI Mean [+ or -] SD 0.31 [+ or -] 0.02 Cholesterol [mg/dl] Mean [+ or -] SD 220.62 [+ or -] 18.42 TG[mg/dl] Mean [+ or -] SD 141.28 [+ or -] 19.78 HDL-Cholesterol [mg/dl] Mean [+ or -] SD 47.72 [+ or -] 3.27 LDL- Cholesterol [mg/dl] Mean [+ or -] SD 143.51 [+ or -] 16.9 Cholesterol : HDL-Cholesterol ratio Mean 3.04 [+ or -] 0.42 [+ or -] SD HDL:LDL ratioMean [+ or -] SD 3.04 [+ or -] 0.42 VLDL [mg/dl] Mean [+ or -] SD 28.27 [+ or -] 3.88 Ghrelin [pg/ml] Mean [+ or -] SD 138.22 [+ or -] 38.40 Omentin1 [ng/ml] Mean [+ or -] SD 252.45 [+ or -] 33.39 Characteristic 3 months [n=60] BMI [Kg/[m.sup.2]] Mean [+ or -] SD 31.91 [+ or -] 2.42 WHR Mean [+ or -] SD 0.85 [+ or -] 0.02 Fasting insulin [[micro]u/ml] Mean [+ or -] 17.76 [+ or -] 6.66 SD Fasting blood glucose [mg/dl] Mean [+ or -] 84.57 [+ or -] 7.18 SD HOMA Mean [+ or -] SD 3.72 [+ or -] 1.51 HOMA [beta]-cell % Mean [+ or -] SD 316.27 [+ or -] 132.42 QUICKI Mean [+ or -] SD 0.33 [+ or -] 0.02 Cholesterol [mg/dl] Mean [+ or -] SD 218.90 [+ or -] 15.89 TG[mg/dl] Mean [+ or -] SD 138.87 [+ or -] 18.45 HDL-Cholesterol [mg/dl] Mean [+ or -] SD 50.12 [+ or -] 4.12 LDL- Cholesterol [mg/dl] Mean [+ or -] SD 141.64 [+ or -] 13.92 Cholesterol : HDL-Cholesterol ratio Mean 2.74 [+ or -] 0.42 [+ or -] SD HDL:LDL ratioMean [+ or -] SD 2.94 [+ or -] 0.42 VLDL [mg/dl] Mean [+ or -] SD 27.74 [+ or -] 3.66 Ghrelin [pg/ml] Mean [+ or -] SD 156.63 [+ or -] 58.36 Omentin1 [ng/ml] Mean [+ or -] SD 278.60 [+ or -] 25.90 Characteristic p value BMI [Kg/[m.sup.2]] Mean [+ or -] SD <0.005 WHR Mean [+ or -] SD <0.01 Fasting insulin [[micro]u/ml] Mean [+ or -] <0.05 SD Fasting blood glucose [mg/dl] Mean [+ or -] >0.05 SD HOMA Mean [+ or -] SD <0.01 HOMA [beta]-cell % Mean [+ or -] SD <0.05 QUICKI Mean [+ or -] SD <0.05 Cholesterol [mg/dl] Mean [+ or -] SD >0.05 TG[mg/dl] Mean [+ or -] SD >0.05 HDL-Cholesterol [mg/dl] Mean [+ or -] SD <0.05 LDL- Cholesterol [mg/dl] Mean [+ or -] SD >0.05 Cholesterol : HDL-Cholesterol ratio Mean <0.05 [+ or -] SD HDL:LDL ratioMean [+ or -] SD <0.05 VLDL [mg/dl] Mean [+ or -] SD <0.05 Ghrelin [pg/ml] Mean [+ or -] SD <0.01 Omentin1 [ng/ml] Mean [+ or -] SD <0.05 Table 2: The effects of metformin in PCOS patients on the omentin1 ratios Characteristics 0 months [n=60] omentin1 : Insulin ratio 14.57 [+ or -] 7.44 Mean [+ or -] SD omentin1 :HOMA ratio 68.91 [+ or -] 38.01 Mean [+ or -] SD omentin1 : HOMA [beta]-cell% 0.87 [+ or -] 0.50 ratio Mean [+ or -] SD Characteristics 3 months [n=60] p value omentin1 : Insulin ratio 20.45 [+ or -] 4.50 <0.01 Mean [+ or -] SD omentin1 :HOMA ratio 80.30 [+ or -] 36.31 <0.01 Mean [+ or -] SD omentin1 : HOMA [beta]-cell% 1.29 [+ or -] 0.54 <0.05 ratio Mean [+ or -] SD Table 3: Baseline Pearson correlations coefficients of omentin-1 levels with various metabolic and hormonal parameters in patients with PCOS. Omentin-1[ng/ ml] p value Variable Correlation BMI [Kg/[m.sup.2]] -0.435 <0.001 Fasting insulin[[micro]U/ml] -0.424 <0.001 HOMA -0.415 <0.001 HOMA [beta]-cell% -0.358 <0.05 QUICKI UQICKI 0.497 <0.001 LDL [mg/dl] -0.590 <0.05 Ghrelin [pg/ml] 0.511 <0.001 Table 4: Baseline Pearson correlations coefficients of ghrelin levels with various metabolic and hormonal parameters in patients with PCOS. Variable Omentin-1 [ng/ml] p value Correlation BMI [Kg/[m.sup.2]] -0.665 >0.001 Fasting insulin[[micro]U/ml] -0.897 >0.001 HOMA -0.871 >0.001 HOMA [beta]-cell% -0.683 >0.001 Cholesterol [mg/dl] -0.641 >0.01 TG [mg/dl] -0.443 >0.01 LDL-cholesterol [mg/dl] -0.656 >0.01 LDL/HDL ratio -0.643 >0.01 Cholesterol/HDL ratio -0.638 >0. 01 QUICKI 0.851 >0.001
|Printer friendly Cite/link Email Feedback|
|Title Annotation:||polycystic ovary syndrome|
|Author:||Shaker, Mahmud; Mashhadani, Zohair I. AL-; Mehdi, Atheer A.|
|Publication:||Oman Medical Journal|
|Date:||Oct 1, 2010|
|Previous Article:||Serum [gamma]-glutamyltransferase as oxidative stress marker in pre-and postmenopausal Iraqi women.|
|Next Article:||Resistance pattern of ciprofloxacin against different pathogens.|