Deconstructing Triglyceride Glucose-Body Mass Index in Normal-Weight Women with Polyendocrine Metabolic Ovarian Syndrome

OBJECTIVE To study the biological pathways underlying the triglyceride glucose-body mass index, calculated as natural logarithm (plasma triglyceride [mg/dL] × fasting blood glucose [mg/dL]/2) × body mass index, in normal-weight women with polyendocrine metabolic ovarian syndrome and age-/body mass index-matched normoandrogenic ovulatory (control) women, and to determine whether the triglyceride glucose-body mass index in such women is a useful clinical predictor of reduced in vitro fertilization pregnancy outcome. DESIGN Retrospective cohort study SUBJECTS: Twenty-one normal-weight women with polyendocrine metabolic ovarian syndrome and 19 age- and body mass index-matched controls. EXPOSURE All women underwent fasting circulating metabolic/androgenic determinations. MAIN OUTCOME MEASURE(S) The triglyceride glucose-body mass index was compared between women with polyendocrine metabolic ovarian syndrome and age-/body mass index-matched controls and correlated with metabolic/androgenic outcomes. RESULTS Serum luteinizing hormone/androgen levels and fasting serum triglyceride/insulin levels were significantly greater in women with polyendocrine metabolic ovarian syndrome than controls (luteinizing hormone/androgen levels, P<0.005 all values; triglyceride, P=0.028; insulin, P=0.037). Adipose insulin resistance also was increased in women with polyendocrine metabolic ovarian syndrome versus controls (P < 0.005). Triglyceride glucose-body mass index and homeostasis model assessment of insulin resistance, however, were not significantly different by female type. In multivariable linear regression, triglyceride glucose-body mass index was unassociated with polyendocrine metabolic ovarian syndrome, serum free testosterone or fasting serum insulin levels. Instead, in all women combined, higher triglyceride glucose-body mass index levels were associated with greater adipose insulin resistance (P=0.01), higher serum non-high-density lipoprotein cholesterol (P=0.02), and lower serum high-density lipoprotein cholesterol (P=0.02) levels. CONCLUSION Adipose insulin resistance accompanying altered lipid metabolism underlies the triglyceride glucose-body mass index of normal-weight women with polyendocrine metabolic ovarian syndrome and age-/body mass index-matched controls. The triglyceride glucose-body mass index, however, may have limited utility in predicting reduced in vitro fertilization pregnancy outcome in normal-weight women with polyendocrine metabolic ovarian syndrome, although confirmation in similar cohorts undergoing in vitro fertilization is needed.