Cellular effects of<unk> <unk>  has been shown to bind to the surface of a number of cell types such as neuronal, endothelial, fibroblast and renal tubular, at nanomolar concentrations to a receptor that is likely G-protein-coupled. The signal activates Ca2+-dependent intracellular signaling pathways such as MAPK, PLCγ, and PKC, leading to upregulation of a range of transcription factors as well as eNOS and Na+K+ATPase activities. The latter two enzymes are known to have reduced activities in patients with type I diabetes and have been implicated in the development of long-term complications of type I diabetes such as peripheral and autonomic neuropathy. In vivo studies in animal models of type 1 diabetes have established that<unk>  administration results in significant improvements in nerve and kidney function. Thus, in animals with early signs of diabetes-induced neuropathy,<unk>  treatment in replacement dosage results in improved peripheral nerve function, as evidenced by increased nerve conduction velocity, increased nerve Na+,K+ ATPase activity, and significant amelioration of nerve structural changes. Likewise,<unk>  administration in animals that had<unk>  deficiency (type 1 model) with nephropathy improves renal function and structure; it decreases urinary albumin excretion and prevents or decreases diabetes-induced glomerular changes secondary to mesangial matrix expansion.<unk>  also has been reported to have anti-inflammatory effects as well as aid repair of smooth muscle cells. A recent epidemiologic study suggests a U-shaped relationship between<unk>  levels and risk of cardiovascular disease.
C-peptide
Leptin
Glucagon-like peptide-1
Insulin index
Insulin tolerance test
Adiponectin
Ghrelin
Nesfatin-1