Adiponectin, a new member of the family of soluble defense collagens, negatively regulates the growth of myelomonocytic progenitors and the functions of macrophages

Abstract

We investigated the functions of adiponectin, an adipocyte-specific secretory protein and a new member of the family of soluble defense collagens, in hematopoiesis and immune responses. Adiponectin suppressed colony formation from colony-forming units (CFU)—granulocyte-macrophage, CFU-macrophage, and CFU-granulocyte, whereas it had no effect on that of burst-forming units—erythroid or mixed erythroid-myeloid CFU. In addition, adiponectin inhibited proliferation of 4 of 9 myeloid cell lines but did not suppress proliferation of erythroid or lymphoid cell lines except for one cell line. These results suggest that adiponectin predominantly inhibits proliferation of myelomonocytic lineage cells. At least one mechanism of the growth inhibition is induction of apoptosis because treatment of acute myelomonocytic leukemia lines with adiponectin induced the appearance of subdiploid peaks and oligonucleosomal DNA fragmentation. Aside from inhibiting growth of myelomonocytic progenitors, adiponectin suppressed mature macrophage functions. Treatment of cultured macrophages with adiponectin significantly inhibited their phagocytic activity and their lipopolysaccharide-induced production of tumor necrosis factor α. Suppression of phagocytosis by adiponectin is mediated by one of the complement C1q receptors, C1qRp, because this function was completely abrogated by the addition of an anti-C1qRp monoclonal antibody. These observations suggest that adiponectin is an important negative regulator in hematopoiesis and immune systems and raise the possibility that it may be involved in ending inflammatory responses through its inhibitory functions.

Decreased muscle mass is not an independent risk factor for metabolic syndrome in Korean population aged 70 or older

“…Previous studies have proven that fat mass, especially visceral fat mass, is associated with inflammatory markers and metabolic parameters. [29][30][31] Consistent with those studies, our study showed that body fat was related to the MetS and its components, independent of muscle mass and other potential confounders. However, our findings did not support that LMM is an independent risk factor for MetS.…”

CEACAM1 loss links inflammation to insulin resistance in obesity and non-alcoholic steatohepatitis (NASH)

“…Neither the insulin sensitizing effect of adiponectin nor its anti-inflammatory effect in both humans and rodents is disputable. The mechanistic underpinning of adiponectin function includes: 1) Promoting the M2 anti-inflammatory polarization of macrophages and their phagocytic activity against apoptotic cells [78,79]; 2) Modulating T cells activation by inducing adiponectin receptors expression on the surface of T cells after antigen stimulation, followed by apoptosis-mediated suppression of antigen specific T cells expansion [80]; 3) Modulating the inflammatory function of natural killer (NK) cells by suppressing their Toll Like Receptor (TLR)-mediated interferon gamma (IFNγ) production without affecting their cytotoxicity [80]; 4) Suppressing transcription of TNFα, IL6 and other pro-inflammatory factors by inhibiting the IKKβ/NF-κB signaling inflammatory pathways [81][82][83][84]; 5) Increasing PPARγ2 expression in adipocytes [82]; and 6) Inducing IL10 expression [85,86].…”

Adiponectin inhibits the growth and peritoneal metastasis of gastric cancer through its specific membrane receptors AdipoR1 and AdipoR2

“…Adiponectin acts as an antiatherogenic hormone through the inhibition of vascular smooth muscle cell proliferation, as well as macrophage functions. (20,21) Adiponectin also has an antidiabetic action through the modulation of glucose and fatty acid metabolism and insulin sensitivity. (22)(23)(24) In fact, the circulating level of adiponectin has been reported to be inversely related to body mass index (BMI) (25)(26)(27) and to be reduced in conditions of insulin resistance such as visceral obesity and type 2 diabetes.…”