Adiponectin is an endocrine factor involving regulation of glucose and lipid metabolism, energy consumption, inflammatory response, immune response, cardiovascular function, and reproduction. In addition, adiponectin also promotes the proliferation and differentiation of osteoblasts and inhibits the formation of osteoclasts, which plays a positive role in the development and maintenance of bone. This review systematically introduces the fluctuation and secretion pattern of serum adiponectin in women from the fetal stage to post-menopause. It discusses the role of adiponectin in the regulation of female body composition and bone mineral density. At the maternal-fetal interface, adiponectin roles in the placenta and adipose tissue by autocrine/paracrine manner and promotes glucose metabolism and fetal development during the fetal stage. At the neonatal stage, the level of umbilical cord serum adiponectin is 2-3 times as much as adults. Serum adiponectin level is positively correlated with the body weight. In the whole period of childhood, serum adiponectin level is, on the contrary, negatively correlated with body fat percentage. Bone mass and bone density also increase with body weight and are negatively correlated with adiponectin. During puberty, serum adiponectin level does not necessarily relate to the level of estrogen in the body. Visceral fat was a negative predictor of bone mineral density and negatively correlated with serum adiponectin level in obese women. In adulthood, serum adiponectin level is negatively correlated with body weight. Female obesity shows a decrease in serum adiponectin level and a negative correlation with bone mineral density. In post-menopause, while estrogen level decreases, serum adiponectin levels in women arise. In summary, increasing body fat percentage affects serum adiponectin level in the whole life of women. Low serum adiponectin level accompanied with the decrease of estrogen level causes an increased risk of developing osteoporosis. |