ABCA1 and ABCG1 expression in the small intestine of type 2 diabetic rats.

OBJECTIVE: Inflammation of the small intestine may occur in type 2 diabetes. This study aimed to investigate whether ATP-binding cassette transporter A1 (ABCA1) and G1 (ABCG1) were altered in chronic inflammation of the small intestine of type 2 diabetic rats. METHODS: Thirty-two male Sprague-Dawley rats were used. Eight rats in the control group were fed with regular chow, and 24 rats were fed a high-fat diet and injected with a single low dose of streptozotocin. All of the control rats and diabetic rats were bred for 10 months. Immunohistochemistry detected ABCA1 and ABCG1 in the small intestine in all the rats. RESULTS: Hematoxylin-eosin staining showed chronic inflammation in the small intestine of the diabetic rats. Immunohistochemistry staining showed that alteration of ABCA1 and ABCG1 was different in the inflammatory and epithelial cells. Quantitative analysis showed that the overall expression of ABCA1 and ABCG1 increased in the diabetic rats compared to the control rats. Both ABCA1 and ABCG1 were enriched in the inflammatory cells of the small intestine in diabetic rats. In the epithelial cells, ABCA1, but not ABCG1, was detected in significantly more diabetic rats than control rats. CONCLUSION: Both ABCA1 and ABCG1 are enriched in chronic inflammation of the small intestine of type 2 diabetic rats. ABCA1, but not ABCG1, is activated in the intestinal epithelial cells of type 2 diabetic rats.

A missense mutation in the arginine-vasopressin neurophysin-II gene causes autosomal dominant neurohypophyseal diabetes insipidus in a Chinese family.

BACKGROUND: Familial neurohypophyseal diabetes insipidus, an autosomal dominant disorder, is mostly caused by mutations in the genes that encode AVP or its intracellular binding protein, neurophysin-II. The mutations lead to aberrant preprohormone processing and progressive destruction of AVP-secreting cells, which gradually manifests a progressive polyuria and polydipsia during early childhood, and a disorder of water homeostasis. OBJECTIVE: We characterized the clinical and biochemical features, and sequenced the AVP neurophysin-II(AVP-NPII) gene of the affected individuals with autosomal dominant neurohypophyseal diabetes insipidus(ADNDI)to determine whether this disease was genetically determined. PATIENTS AND METHODS: We obtained the histories of eight affected and four unaffected family individuals. The diagnosis of ADNDI was established using a water deprivation test and exogenous AVP administration. For molecular analysis, genomic DNA was extracted and the AVP-NPII gene was amplified using polymerase chain reaction and sequenced. RESULTS: The eight affected individuals showed different spectra of age of onsets (7-15 years) and urine volumes (132-253 ml/kg/24 h). All affected individuals responded to vasopressin administration, with a resolution of symptoms and an increase in urine osmolality by more than 50%. The characteristic hyperintense signal in the posterior pituitary on T1-weighted magnetic resonance imaging was absent in six family members and present in one. Sequencing analysis revealed a missense heterozygous mutation 1516G > T (Gly17Val) in exon 2 of the AVP-NPII gene among the ADNDI individuals. CONCLUSIONS: We identified a missense mutation in the AVP-NPII gene and the same mutation showed different spectra of age of onsets and urine volumes in a new Chinese family with ADNDI. The mutation may provide a molecular basis for understanding the characteristics of NPII and add to our knowledge of the pathogenesis of ADNDI, which would allow the presymptomatic diagnosis of asymptomatic subjects.

Analysis of various etiologies of hypertension in patients hospitalized in the endocrinology division.

This research aimed to analyze the clinical data of various etiologies of hypertension in patients hospitalized in the Endocrinology Division. The differences between essential and secondary hypertension were examined to provide a basis for clinical differential diagnosis. The data from all the inpatients with hypertension of unknown origin admitted in the Endocrinology Division of the First Affiliated Hospital of the Zhejiang University School of Medicine from January 2001 to May 2011 were reviewed. The patients were classified into either essential or secondary hypertensive groups. The differentiating parameters of these forms of hypertension were analyzed using the one-factor and multi-factor logistic regression analysis. A total of 1,001 cases were selected in which 346 cases (34.6%) were essential hypertensive and 655 cases (65.4%) were secondary hypertensive. Adrenal hypertension was the primary cause of secondary hypertension, followed by renal artery, central, psychogenic, and renal hypertension as well as others that have not been classified systematically. Using one-factor analysis, significant differences were found among duration of hypertension, age, the onset age, family history of hypertension, diastolic pressure on admission, Cushing syndrome, body mass index (BMI), urine protein, serum creatinine, orthostatic aldosterone, ratio of orthostatic aldosterone to renin activity, incidence of fatty liver displayed by type-B ultrasound, and computed tomography adrenal masses incidence (P < 0.05). Multi-factor regression analysis showed that family history of hypertension (OR = 7.196) and BMI above the normal range (OR = 15.124) were the independent factors that predicted essential hypertension, but failed to determine any other valid predictors of secondary causes except adrenal masses (OR = 10.114), orthostatic aldosterone value >200 pg/ml (OR = 9.742), and a ratio of orthostatic aldosterone and renin activity >40 (OR = 4.723).