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Diabetic nephropathy(DN) is the most common cause of chronic kidney disease, leading to end-stage renal disease (ESRD) and cardiovascular disease (CVD). The overall number of patients with DN will continue to increase in parallel with the increasing global pandemic of type 2 diabetes. The detection of albuminuria is most important for diagnosis of early stage of DN, and also estimated glomerular filtration rate (eGFR) should be assessed, because both albuminuria and reduction of GFR are recognized as the independent risk factor for progression of ESRD and initiation of CVD, respectively. Based on landmark clinical trials, both DN and CVD have become preventable by controlling conventional factors, including hyperglycemia targeting HbA1c7.0%, hypertenstion using renin angiotensin system inhibitors, dyslipidemia using statins or fibrates, and multifactorial treatment.

Suppressing food intake is the most well-known central nervous action of glucagon-like peptide-1 (GLP-1). Neurons expressing preproglucagon (PPG) in the nucleus tractus solitarius (NTS) are the only source of "central" GLP-1, and they project to the hypothalamus. Recently, properties of these PPG-neurons have been revealed using transgenic mice expressing fluorescent protein under control of the PPG promoter; whereas they are directly responsible to leptin but not to GLP-1, they can be the second-order neurons of vagal afferents. "Peripheral" GLP-1 released from intestinal L-cells may possess central nervous action through the vagal afferent fibers. The question remains whether food intake suppression due to "peripheral" GLP-1 depends on "central" one. The action is being applied to anti-obesity therapy.