The cut-off value for HOMA-IR discriminating the insulin resistance based on the SHBG level in women with polycystic ovary syndrome

Biernacka-Bartnik, Aleksandra; Kocełak, Piotr; Owczarek, Aleksander; Choręza, Piotr Stanisław; Markuszewski, Leszek; Madej, Paweł; Puzianowska-Kuźnicka, Monika; Chudek, Jerzy; Olszanecka-Glinianowicz, Magdalena

doi:10.3389/fmed.2023.1100547

Cited by 10 publications

(6 citation statements)

References 37 publications

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“…Insulin resistance associated with PCO improves with appropriate treatment of the disease; however, in addition to the classical OGTT measurement, a simple parameter that correlates well with the daily changes of serum insulin levels would be helpful to monitor long term changes of carbohydrate metabolism. Based on the literature data, SHBG seemed to be a promising parameter, as an inverse linear correlation between HOMA index and SHBG was seen in some patients with PCO syndrome [18][19][20], while others did not suggest it as a marker in PCO syndrome due to the excessive variability of SHBG [21]. In the current investigation, we aimed to determine whether an inverse linear correlation could also be seen in women with normal fasting insulin, accompanied by normal/low body weight phenotype PCO syndrome.…”

Section: Discussionmentioning

confidence: 99%

“…There have been several publications on the relationship between insulin sensitivity (the HOMA index) and serum SHBG levels. Studies have demonstrated an inverse linear correlation between the Homeostasis Model Assessment (HOMA) index and SHBG, which makes SHBG a suitable marker for metabolic characterization [18][19][20]. However, there has also been research that has not recommended the use of SHBG as a marker in PCO syndrome due to its high variability [21].…”

Section: Of 10mentioning

confidence: 99%

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SHBG Levels Do Not Correlate with Insulin Levels in PCOS with Appropriate Fasting Insulin Sensitivity

Tűű,

Nas,

Török

et al. 2024

JCM

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Introduction: There are several phenotypes of polycystic ovarian syndrome (PCOS), and the different phenotypes may differ metabolically. Methods: In the present retrospective study, women with PCOS having normal fasting insulin sensitivity (n = 88) were compared with women with PCOS showing impaired insulin sensitivity (n = 46) using the HPCOS (Hungarian Polycystic ovarian syndrome) database. Results: The impaired insulin sensitivity group has significantly higher body mass index (BMI) and HOMA index than the normal fasting insulin sensitivity group (BMI (kg/m2): 22.0 vs. 28.1, p < 0.0001, HOMA index: 0.96 vs. 2.38, p < 0.0001). The sex hormone binding globulin (SHBG) level was significantly lower, and the free androgen index proved itself significantly higher in the impaired insulin sensitivity group (p < 0.05). Linear regression analysis showed a negative association of BMI with SHBG levels in both groups, while BMI had a positive correlation with insulin concentrations in both groups. However, the SHBG levels were negatively associated with insulin concentrations in the impaired insulin sensitivity group, but this inverse association could not be observed in the normal fasting insulin sensitivity group. Conclusions: The inverse linear correlation of SHBG with HOMA index and serum insulin level is not evident in all PCO syndrome phenotypes, thus SHBG has limited applicability for characterizing carbohydrate metabolism and serum insulin sensitivity.

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Section: Discussionmentioning

confidence: 99%

Section: Of 10mentioning

confidence: 99%

SHBG Levels Do Not Correlate with Insulin Levels in PCOS with Appropriate Fasting Insulin Sensitivity

Tűű,

Nas,

Török

et al. 2024

JCM

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“…A reduction in the SHBG concentration, a globulin produced mainly in the liver, is associated with PCOS and is a marker of the severity of hepatic insulin resistance. The expression of SHBG mRNA was found to be negatively correlated with the accumulation of triglycerides in hepatocytes [ 53 ]. ALT, a marker of liver cell injury, was elevated above 19 IU/mL in 35.7% of Low HDL-C subfertile women as compared with 4% of fertile women with a level of HDL-C above 50 mg/mL.…”

Section: Discussionmentioning

confidence: 99%

Subfertility as Overlapping of Nutritional, Endocrine, Immune, and Cardiometabolic Dysregulations—A Study Focused on Biochemical Endophenotypes of Subfertile Couples

Wasilewski,

Wasilewska,

Łukaszewicz-Zając

et al. 2023

JCM

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Subfertility is a global health issue, and as many as 30% of cases are attributed to unexplained reasons. A hypercaloric, high-fat diet stimulates the expansion of pro-inflammatory gut microbiota with a consequent rise in circulating lipopolysaccharides. Adverse gut microbiota remodeling can exacerbate insulin resistance, while sex and thyroid hormones may influence the variability in gut microbiota. This cross-sectional study included 150 participants and was designed to determine a biochemical, nutritional-related pattern that may distinguish subfertile from fertile individuals and couples. A panel of 28 biomarkers was assessed. Four biochemical phenotypes of unexplained subfertility were found, including two metabolic and two immune, when assessed using binary logistic regression models. Two phenotypes were distinguished in women: cardio-metabolic with atherogenic dyslipidemia (LowHDL-cholesterol: OR = 10.9; p < 0.05) and autoimmune thyroid disorder (Highanti-thyroid-peroxidase: OR = 5.5; p < 0.05) and two in men: hepato-metabolic with elevated liver injury enzymes (HighHOMA-IR: OR = 6.1; p < 0.05) and immune type-2 response (HighIgE: OR = 6.4; p < 0.05). The chances of a couple’s subfertility rose with the number of laboratory components of metabolic syndrome in the couple (OR = 1.7; p < 0.05) and if at least one partner had an elevated total IgE level (>100 kU/L) (OR = 6.5; p < 0.05). This study found that unexplained subfertility may be accompanied by mutually overlapping immune and metabolic dysregulations in individuals and couples. We propose one-time laboratory diagnostics taking into account the lipid profile, insulin resistance, anti-thyroid-peroxidase, and total IgE in both males and females with unexplained subfertility. This may allow for a one-time assessment of targeted medical and nutritional interventions and help optimize patients’ health. The gut–organ axes related to subfertility are discussed in the context of the obtained results.

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“…The Homeostatic Model Assessment of Insulin Resistance (HOMA-IR) is an easy and non-invasive way to figure out how sensitive your body is to insulin [ 24 ]. The PCOS patients were classified as insulin resistant (HOMA IR ≥ 2.0, n = 35) or non-insulin resistant (HOMA IR < 1.9, n = 27) using the Homeostasis Model Assessment of Insulin Resistance (HOMA IR) [ 25 ]. If the value is greater than 2.0, it suggests that a person’s body might be resistant to insulin.…”

Section: Methodsmentioning

confidence: 99%

Association of FTO gene variant rs9939609 with polycystic ovary syndrome from Gujarat, India

Chaudhary,

Patel,

Jain

et al. 2023

BMC Med Genomics

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Background Polycystic ovary syndrome is a multifactorial endocrine disorder impacting women of reproductive age. Variations within the FTO gene have been linked to both obesity and type 2 diabetes mellitus. Given that PCOS is frequently associated with obesity and compromised glucose tolerance, we investigated the prevalence of the rs9939609 variant within the FTO gene among women diagnosed with PCOS and a control group. Our aim is to uncover potential correlations between this genetic variant, metabolic attributes, and endocrine markers within the Gujarat province of India. Method We enrolled a total of 114 participants, (62 individuals diagnosed with PCOS and 52 healthy controls). DNA extraction from venous blood was conducted for all participants. The rs9939609 polymorphism was investigated through tetra-primer amplification refractory mutation system-polymerase chain reaction. Furthermore, we performed biochemical assessments to quantify levels of estradiol, luteinizing hormone (LH), follicle-stimulating hormone (FSH), thyroid-stimulating hormone (TSH), total testosterone, prolactin (PRL), and Dehydroepiandrosterone sulfate (DHEAS). Statistical analyses were carried out utilizing SPSS version 21 (IBM, USA). Results The present study did not reveal any noteworthy association between cases and controls. The frequencies of genotypes and alleles within the cohorts displayed no statistically significant differences (p = 0.25, p = 0.68, and p = 0.78, respectively). The dominant model indicated a modest risk (OR:1.13, 95%CI: 0.55 to 2.38) toward PCOS development. There was a noticeable statistical difference observed in the levels of total testosterone, DHEAS, and BMI between the case and control groups (p < 0.002, p < 0.0002, p < 0.0008). However, no variations in clinical variables were observed among genotypes within the PCOS group. Conclusion This is the first study to investigate the association of FTO gene polymorphism and PCOS in Gujarati population. Our study findings indicate that the FTO gene variant is not directly linked to the onset of PCOS. However, it appears to exert an influence on metabolic factors such as obesity and insulin resistance. Notably, our results suggest that insulin resistance is more frequently observed among PCOS patients who are obese, as compared to those with non-obese PCOS patients.

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The cut-off value for HOMA-IR discriminating the insulin resistance based on the SHBG level in women with polycystic ovary syndrome

Cited by 10 publications

References 37 publications

SHBG Levels Do Not Correlate with Insulin Levels in PCOS with Appropriate Fasting Insulin Sensitivity

SHBG Levels Do Not Correlate with Insulin Levels in PCOS with Appropriate Fasting Insulin Sensitivity

Subfertility as Overlapping of Nutritional, Endocrine, Immune, and Cardiometabolic Dysregulations—A Study Focused on Biochemical Endophenotypes of Subfertile Couples

Association of FTO gene variant rs9939609 with polycystic ovary syndrome from Gujarat, India

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