Table 1.

Summary of the body composition and fat distribution differences in man and women and the main endocrine and hormonal imbalances that occur as a result of obesity in men and women.

	In Females	In Males
Body composition and fat distribution	Body fat percentage of 15%, with the total adipose tissue volume being 12% of the total body weight [17] Gluteofemoral fat and then, after menopause, abdominal fat [27] Essential fat of 5–9%, encompassing sex-specific fat [22]	Body fat percentage of 12%, with the total adipose tissue volume being 4% of the total body weight [17] Abdominal fat [22] Greater visceral adiposity → increased postprandial insulin, free fatty acids, and triglycerides [28]
Hormonal Imbalances	In Females	In Males
Obesity	Obesity → irregular menstrual cycles, miscarriage rates, anovulation, and adverse neonatal and maternal outcomes [68]; hirsutism [69]; compromission of oocyte quality and development [78]; prolonged gestational periods and gestational diabetes [79]; and higher androgen levels [64] Higher total and free testosterone levels but lower levels of androstenedione and SHBG [64] → visceral white adipose tissue hypertrophy and/or hyperplasia → risk of IR and metabolic syndrome in hyperandrogenic women Adipose tissue and imbalance of adipokine levels → PCOS	Adipocyte hypertrophy and hyperplasia through adipokine secretion [34] → impact on HPG axis [36] Relationship between thyroid hormones, leptin, and reproductive function → male infertility [41] Erectile dysfunction and elevated scrotal temperature → male infertility [42] Testosterone conversion to estradiol → secondary hypogonadism [50]
Hyperinsulinemia, leptin, and insulin resistance (IR)	Reproductive age: greater insulin sensitivity, increased stimulated insulin secretion, and lower fasting glucose and HbA1c levels [86] During menopause: increased blood pressure and LDL cholesterol and HbA1c levels → body fat distribution → impaired glucose tolerance (IGT) [86] Increased insulin stimulates theca cells to produce androgens → extradiol synthesis [80] PCOS: increased insulin → androgen production, contributing to follicular arrest and anovulation and inhibition of SHBG production → increased testosterone [89] PCOS: increased insulin → enhancing LH pulse amplitude, increasing sensitivity to gonadotropin-releasing hormone [90] → P450c17α enzyme → increasing adrenal androgen production → hyperandrogenism [91] Increased leptin → imbalance of plasma female sex hormone levels [87] and disruption of oocyte development [88] Obesity-related hyperinsulinemia and IR → menstrual irregularities, hyperandrogenism, and alterations in steroidogenesis (also in non-obese) [92]	Elevated insulin → Decreased SHBG [44] and impact on fertility indicators [51] Increased leptin secretion → inhibition testosterone production [35] Fat mass → promotion of testosterone conversion to estradiol [44] → secondary hypogonadism [50] Low testosterone levels → bone density, fat distribution, muscle mass, red blood cell production [45,46], IR, and obesity [44]
Cortisol	↑ Cortisol in obesity → visceral fat accumulation, IR, and an increased risk of metabolic syndrome [95] Premenopausal women with obesity with elevated WHR and tendency to visceral fat accumulation → increased urinary cortisol and normal dexamethasone inhibition of cortisol secretion [96] Responses to physical or mental stressors → increasing serum cortisol levels, with no influence on prolactin or GH [96] Androgynous obesity in women → increased sensitivity along HPA axis → increased cortisol secretion → contribution to abnormal fat depot distribution and metabolic abnormalities	↑ Cortisol → visceral fat accumulation, insulin resistance, and an elevated risk of metabolic syndrome [55] Stress input and elevated cortisol in obesity → hypothalamic–pituitary–adrenal (HPA) axis dysregulation and impact on reductions in IGF-I and testosterone levels [55]
Thyroid hormones	Fluctuation in TSH levels correlated to leptin concentrations [53,55,83] → thyroid dysfunction → IR, dyslipidemia, and cardiovascular complications [70] Altered thyroid function → impact on energy expenditure, fat metabolism, and weight management [71]	Increased TSH levels and triiodothyronine (T3), unchanged T4 levels [52,55] → thyroid hormone resistance → increased TSH and fT3 secretion Altered leptin production → impact on TSH regulation through leptin resistance [54] Positive correlation between BMI and TSH levels [55]
Dyslipidemia		Oxidative stress → quality of male germ cells and infertility Modification in structures and functions of testes and epididymis, energy metabolism, and spermatogenesis [18,46] Acrosomal response and capacitation → hormonal imbalances and erectile disfunction [18,46]
Oxidative stress and inflammation	Imbalance between the production of ROS and antioxidant defenses → compromission of follicle development, oocyte maturation, and embryo and placental growth [93] Disruptions in leptin during pregnancy → impediment of oocyte development [79] Menstrual irregularities, infertility, intrauterine growth restriction, preeclampsia, recurrent miscarriages, and premature births [95]	Elevated ROS levels in sperm Contribution to IR and leptin dysregulation [42,58]
Gut microbiota composition	PCOS → reduces alpha and beta diversity [96] Dysbiosis and Lactobacillus deficiency → interference with assisted reproduction treatments [98] Gram-negative bacteria, Chlamydia trachomatis, and Gardnerella vaginalis in cervical flora → infertility problems [97]	Increased lipopolysaccharides → promotion of obesity and IR [59], mediated by TNF-α, IL-6, and leptin from adipose tissue Dysbiosis → impact on blood–testis barrier development and intratesticular testosterone levels → Sertoli cell development and maturation [63]

↑ increase, → leads to.