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Objective The impact of the clustering of metabolic factors on chronic kidney disease (CKD) in non-obese individuals remains unclear. Methods We conducted a follow-up study of 23,894 Japanese adults (age, 18-69 years) who continuously received annual health examinations between 2000 and 2011. Obesity, high blood pressure, high triglycerides, low high-density lipoprotein (HDL) cholesterol and high fasting blood sugar were defined as metabolic factors, and CKD was defined as renal dysfunction (estimated glomerular filtration rate: <60 mL/min/1.73 m 2 ) or proteinuria (dipstick test: ! 1+). The association between the clustering of metabolic factors and CKD was assessed based on the presence or absence of obesity using a Cox proportional hazard model. Results Of 2,867 subjects with ! 3 metabolic factors, 650 (22.7%) were non-obese. These individuals were older and had higher metabolic risks than their obese counterparts at baseline. Among the entire cohort of 23,894 subjects, 1,764 developed renal dysfunction and 904 developed proteinuria during an average followup period of 7.8 years. The cumulative incidence of renal dysfunction was higher (22.1% vs. 16.1%), whereas that of proteinuria was lower (10.5% vs. 14.4%), among the non-obese subjects with ! 3 metabolic factors than the obese subjects with ! 3 metabolic factors after 11 years. The adjusted relative risk (RR) (95% confidence interval) of renal dysfunction was 1.54 (1.34-1.77) and 1.67 (1.35-2.07) for the obese and nonobese subjects with ! 3 metabolic factors, respectively. Conclusion Non-obese subjects with ! 3 metabolic factors, who are missed based on the essential criterion of obesity for metabolic syndrome, may have an equal or slightly higher risk of renal dysfunction than obese subjects with ! 3 metabolic factors.

To clarify the effect of islet hormones on pancreatic ductular cell function, we measured the exocrine secretion elicited by 10 pM secretin in the presence or absence of islet hormones using an isolated perfused rat pancreas model. Insulin significantly increased secretin-stimulated pancreatic juice secretion, but not protein secretion. The potentiating effect of insulin on pancreatic juice secretion was concentration-dependent, and the maximal effect was observed with 1 microM insulin. Ouabain, a specific Na+,K(+)-ATPase inhibitor, caused concentration-dependent inhibition of the potentiating effect of insulin without affecting secretin action. Glucagon (100 nM) significantly inhibited secretin-stimulated pancreatic juice secretion and also tended to inhibit protein secretion. A somatostatin analog, SMS 201-995 (10 nM) significantly inhibited both the pancreatic juice and protein secretion stimulated by secretin. The inhibitory effect of SMS 201-995 was concentration-dependent and was maximal at 1-10 nM. These results demonstrate that insulin potentiates the secretory response to secretin, at least partly by increasing Na+,K(+)-ATPase activity, whereas glucagon and somatostatin inhibit this response. Thus, pancreatic islet hormones regulate the secretory function of pancreatic ductular and centroacinar cells.

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Background: Carcinoid tumors are usually considered to have a low degree of malignancy and show slow progression. One of the factors indicating the malignancy of these tumors is their size, and small ampullary carcinoid tumors have been sometimes treated by endoscopic resection.