Obesity, but not hyperandrogenism or insulin resistance, predicts skeletal muscle mass in reproductive‐aged women with polycystic ovary syndrome: A systematic review and meta‐analysis of 45 observational studies

Abstract

Women with polycystic ovary syndrome (PCOS) exhibit reduced muscle insulinmediated glucose uptake, potentially attributed to altered muscle mass; however, this is inconclusive. Altered muscle mass may aggravate PCOS complications. Our systematic review and meta-analysis evaluated whether PCOS alters muscle mass and function. Databases (MEDLINE, Web of Science, Scopus) were searched through September 2, 2020, for studies documenting skeletal muscle mass (lean tissue mass) and function (strength) in PCOS and control groups. The primary outcome was total lean body mass (LBM) or fat-free mass (FFM). Data were pooled by random-effects models and expressed as mean differences and 95% confidence intervals. Forty-five studies (n = 3676 participants) were eligible. Women with PCOS had increased total (0.83 [0.08,1.58] kg; p = 0.03; I 2 = 72.0%) yet comparable trunk (0.84 [−0.37,2.05] kg; p = 0.15; I 2 = 73.0%) LBM or FFM versus controls. Results of metaregression analyses showed no associations between mean differences between groups in total testosterone or homeostatic model assessment of insulin resistance and total or trunk LBM or FFM (All: p ≥ 0.75). Mean differences in body mass index (BMI) were associated with total (0.65 [0.23,1.06] kg; p < 0.01; I 2 = 56.9%) and trunk (0.56 [0.11,1.01] kg; p = 0.02; I 2 = 42.8%) LBM or FFM. The PCOS subgroup with BMI ≥ 25 kg/m 2 had greater total LBM or FFM versus controls (1.58 [0.82,2.34] kg; p < 0.01; I 2 = 64.0%) unlike the PCOS subgroup with BMI < 25 kg/m 2 (−0.45 [−1.94,1.05] kg; p = 0.53; I 2 = 69.5%). Appendicular lean mass and muscle strength data were contradictory and described narratively, as meta-analyses were impossible.

Higher Muscle Mass Protects Women with Gestational Diabetes Mellitus from Progression to Type 2 Diabetes Mellitus

“…To better understand the relationship between muscle mass and the risk of T2DM, we need to clarify the factors that contribute to increased muscle mass in women with PCOS (e.g., androgens, higher body weight, and/or fat mass). A recent meta-analysis reported that higher total and trunk lean tissue mass were observed in a subgroup of women with PCOS who are BMI ≥25 kg/m 2 , which were attributed to overweight and obesity, but not androgen or insulin resistance [ 36 ]. On the other hand, increases in total or trunk lean mass were not evident in women with BMI <25 kg/m 2 .…”

Insulin resistance in polycystic ovary syndrome across various tissues: an updated review of pathogenesis, evaluation, and treatment

“…In addition, hyperandrogenaemia may increase inflammation by activating nuclear factor kappa B (NF-κB), which in turn affects intracellular enzyme pathways associated with insulin receptors [ 51 ]. A recent meta-analysis suggested that obesity, but not HA or IR, appears to predict skeletal muscle mass in reproductive-aged women with PCOS [ 79 ]. Intramuscular lipid accumulation within muscle cells or between fibres may account for a small percentage of skeletal muscle IR [ 80 ].…”

Metabolic Syndrome and PCOS: Pathogenesis and the Role of Metabolites

“…For example, due to adipose tissue dysfunction, adipocytes secrete non-physiological levels of adipokines, including IL6, IL8, TNF-α, leptin, adiponectin, resistin, lipocalin 2, monocyte chemoattractant protein-1 (MCP1), retinol binding protein-4 (RBP4), and CXC-chemokine ligand 5 (CXCL5), which may be involved in IR [21][22][23][24]. In addition, a recent study has indicated that obesity may function as a better predictor of skeletal muscle mass in PCOS women than hyperandrogenism and IR, which may aggravate PCOS complications [25]. Interestingly, adipose tissue dysfunction can affect follicular development.…”