B-Bridge is pleased to offer the first non-radioactive means of detecting adiponectin from serum/plasma samples, adipocytes or conditioned media.

Obesity, and obesity-related disorders, are reaching alarming proportions in the US, and are on the increase in Europe and Asia. A deeper understanding of the molecular and cellular dynamics of such disorders, and their subsequent amelioration, will have a far-reaching impact on the quality of life of millions of people worldwide.

Adipocytes (fat cells) express a variety of proteins that function in the homeostatic control of glucose and lipid metabolism. Insulin regulates the translocation and secretion of many of these proteins in response to changes in energy balance. Adipocyte complement-related protein of 30 kDa (Acrp30), now known as adiponectin, is a protein whose secretion from adipocytes is enhanced by insulin stimulation.

It has been suggested that the development of non-insulin dependent (Type II) diabetes may involve dysregulation of adiponectin secretion (1). In support of the link between obesity and Type II diabetes, it has been shown that decreased expression of adiponectin correlates with insulin resistance (2,3), and that adiponectin appears to be a potent insulin enhancer linking adipose tissue and whole-body glucose metabolism (4).

Nemet, D., et al. (2002) Relationships among adiponectin and other adipose cytokines, body composition, and fasting insulin in lower socioeconomic middle school children. American Physiological Societyys (APS) Abstracts.

Yamauchi T., et al. (2001) The fat-derived hormone adiponectin reverses insulin resistance associated with both lipoatrophy and obesity. Nature Medicine, Aug;7(8):941-6.

Kubota, N., et al. (2002) Disruption of adiponectin causes insulin resistance and neointimal formation. J Biol Chem. May 24 (epub ahead of print).

Berg A.H., et al. (2001) The adipocyte-secreted protein Acrp30 enhances hepatic insulin action. Nature Medicine, Aug;7(8):947-53.