PubMed · 15084735
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Mitch Leslie. 2004-04-14. Lightheaded.. https://doi.org/10.1126/sageke.2004.15.nf41
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Since interaction between bone and lipid metabolism has been suggested, this study investigated the regulation of bone metabolism by adiponectin, a representative adipokine, by analyzing deficient and overexpressing transgenic mice. We initially confirmed that adiponectin and its receptors were expressed in osteoblastic and osteoclastic cells, indicating that adiponectin can act on bone not only through an endocrine pathway as a hormone secreted from fat tissue, but also through an autocrine/paracrine pathway. There was no abnormality in bone mass or turnover of adiponectin-deficient (Ad-/-) mice, possibly due to an equivalent balance of the two pathways. In the culture of bone marrow cells from the Ad-/- mice, osteogenesis was decreased compared to the wild-type (WT) cell culture, indicating a positive effect of endogenous adiponectin through the autocrine/paracrine pathway. To examine the endocrine action of adiponectin, we analyzed transgenic mice overexpressing adiponectin in the liver, and found no abnormality in the bone. Addition of recombinant adiponectin in cultured osteoprogenitor cells suppressed osteogenesis, suggesting that the direct action of circulating adiponectin was negative for bone formation. In the presence of insulin, however, this suppression was blunted, and adiponectin enhanced the insulin-induced phosphorylations of the main downstream molecule insulin receptor substrate-1 and Akt. These lines of results suggest three distinct adiponectin actions on bone formation: a positive action through the autocrine/paracrine pathway by locally produced adiponectin, a negative action through the direct pathway by circulating adiponectin, and a positive action through the indirect pathway by circulating adiponectin via enhancement of the insulin signaling.
OBJECTIVE: Interleukin-18 (IL-18) is a cytokine with proinflammatory and proatherogenic properties, which might be associated with the development of insulin resistance. In contrast, adiponectin, a protein secreted by adipose tissue, might exert insulin-sensitizing and antiatherogenic effects. The aim of the present study was to analyze the association between serum IL-18 and adiponectin in lean and obese subjects, in relation to insulin resistance. DESIGN: Cross-sectional study. SUBJECTS: One hundred and thirty individuals, 62 lean (body mass index (BMI)<25 kg/m(2), 30 men and 32 women) and 68 with overweight or obesity (BMI>25 kg/m(2), 24 men and 44 women), with normal glucose tolerance and without concomitant diseases. MEASUREMENTS: Oral glucose tolerance test, euglycemic hyperinsulinemic clamp, serum concentrations of IL-18, IL-6, soluble tumor necrosis factor-alpha receptors and adiponectin. RESULTS: Obese subjects had lower insulin sensitivity (M value, P=0.00029) and serum adiponectin (P=0.01) and higher levels of serum IL-18 (P=0.00055). Circulating IL-18 was negatively related to adiponectin (r=-0.31, P=0.00027) and insulin sensitivity (r=-0.33, P=0.00012). Subgroup analysis revealed that these associations were present in the obese (adiponectin, r=-0.38, P=0.0014; M, r=-0.29, P=0.016), but not in lean individuals (r=-0.17, P=0.18 and r=-0.20, P=0.12, respectively). Association of IL-18 with adiponectin remained significant after adjustment for other estimated parameters, including insulin sensitivity. Also, relationship between IL-18 and insulin sensitivity was independent of other estimated parameters. CONCLUSION: Serum IL-18 is inversely related to serum adiponectin, independently of insulin resistance. The relationships of IL-18 with adiponectin and insulin sensitivity are influenced by the presence of overweight/obesity.
OBJECTIVE: Obesity is a risk factor for pre-eclampsia, and adiponectin is an important adipocyte-derived hormone that might protect the endothelium. Recent reports have underlined importance of circulating angiogenic factors for pathophysiology of pre-eclampsia. Here we examined whether adiponectin in conjunction with angiogenic factors plays some roles in the pathophysiology of pre-eclampsia. STUDY DESIGN: We measured serum concentrations of adiponectin and angiogenic factors, vascular endothelial growth factor, placental growth factor, and the soluble vascular endothelial growth factor receptors, soluble fms-like tyrosine Kinase 1 (sFlt-1) and soluble fetal liver kinase 1 (sFlk-1), in women with pre-eclampsia and healthy pregnant women. We also investigated the differences of these factors in overweight and normal-weight patients with pre-eclampsia. RESULTS: Significant correlations were found among the circulating adiponectin and angiogenic factors placental growth factor (R = 0.772, P = .0012) and sFlt-1 (R = 0.787, P = .0005); while, no correlation was found between adiponectin and sFlk-1 (R = 0.3, P = .3434) in patients with pre-eclampsia. Overweight patients with pre-eclampsia showed significantly lower adiponectin levels and a mild imbalance of circulating angiogenic factors, compared with normal-weight patients with pre-eclampsia. CONCLUSION: Overweight women with pre-eclampsia appeared to have lower levels of adiponectin and sFlt1 and higher levels of placental growth factor than women with pre-eclampsia who were of normal weight. These results suggest that hypoadiponectinemia might be involved in the pathophysiology of overweight patients with pre-eclampsia.