pituitrin and Fatty-Liver

High plasma copeptin, a marker of vasopressin (VP) secretion, has been shown to be associated with the metabolic syndrome and development of type 2 diabetes in humans. The present study was designed to determine the long-term influence of plasma VP concentration in a rodent model prone to metabolic dysfunction.. Obese Zucker rats and their lean counterparts were submitted for 4 weeks to one of three protocols inducing different levels of VP. Circulating VP was either reduced by increasing the daily water intake (low-VP), or increased by a chronic i.p. infusion of VP (high-VP). The control rats had normal VP levels that depended on their own regulation of water intake and VP secretion.. Compared with controls with normal VP, lean rats with high-VP had a higher fasting glycaemia after 4 weeks. In obese rats, high-VP promoted hyperinsulinaemia, glucose intolerance, assessed by glucose and insulin tolerance tests, and an impaired response to a pyruvate challenge. Conversely, treatment with a selective arginine vasopressin receptor 1A (V1aR) antagonist reduced glucose intolerance. Low-VP obese rats had unchanged glucose tolerance but exhibited a drastic decrease in liver steatosis compared with control obese rats, associated with low hepatic triacylglycerol and cholesterol content, and reduced expression of hepatic lipogenic genes. These effects were independent of changes in body adiposity, and plasma sodium and osmolality did not differ among groups.. These findings show a causal relationship between the VP-hydration axis and the metabolic risk. Therapeutic perspectives include diet recommendations regarding hydration, but also potential pharmacological interventions targeting the VP V1aR.

Topics: Animals; Antidiuretic Hormone Receptor Antagonists; Blood Glucose; Drinking; Fatty Liver; Glucose Intolerance; Glucose Tolerance Test; Indoles; Male; Obesity; Pyrrolidines; Rats, Zucker; Vasopressins

Non-alcoholic steatohepatitis (NASH) is a serious form of non-alcoholic fatty liver disease (NAFLD), associated with obesity and insulin resistance. Previous studies suggested that intestinal bacteria produced more alcohol in obese mice than lean animals.. To investigate whether alcohol is involved in the pathogenesis of NASH, the expression of inflammation, fibrosis and alcohol metabolism related genes in the liver tissues of NASH patients and normal controls (NCs) were examined by microarray (NASH, n = 7; NC, n = 4) and quantitative real-time PCR (NASH, n = 6; NC, n = 6). Genes related to liver inflammation and fibrosis were found to be elevated in NASH livers compared to normal livers. The most striking finding is the increased gene transcription of alcohol dehydrogenase (ADH) genes, genes for catalase and cytochrome P450 2E1, and aldehyde dehydrogenase genes. Immunoblot analysis confirmed the increased expression of ADH1 and ADH4 in NASH livers (NASH, n = 9; NC, n = 4).. The augmented activity of all the available genes of the pathways for alcohol catabolism suggest that 1) alcohol concentration was elevated in the circulation of NASH patients; 2) there was a high priority for the NASH livers to scavenge alcohol from the circulation. Our data is the first human evidence that suggests alcohol may contribute to the development of NAFLD.

Topics: Adolescent; Alcohol Dehydrogenase; Alcohol Drinking; Alcohols; Child; Cytochrome P-450 CYP2E1; Fatty Liver; Female; Fibrosis; Humans; Immunoblotting; Inflammation; Liver; Male; Neurophysins; Protein Precursors; Vasopressins

Topics: Adult; Antineoplastic Agents; Cytarabine; Fatty Liver; Female; Granulocyte Precursor Cells; Humans; Immunohistochemistry; Leukemia, Myeloid, Acute; Liver; Tomography, X-Ray Computed; Vasopressins

Topics: Adult; Diabetes Insipidus; Diuresis; Fatty Liver; Female; Humans; Liver; Pregnancy; Pregnancy Complications; Vasopressins

Autopsy in a patient with severe hyponatremia showed central pontine myelinolysis. Review of our patients with central pontine myelinolysis and those described in the English literature to data disclosed that 61 percent had documented hyponatremia. While the exact mechanism involving hyponatremia and central pontine myelinolysis cannot be defined, a circumstantial relationship is apparent. The purpose of this paper is to emphasize this relationship and to suggest that the possibility of central pontine myelinolysis be considered in any patient with hyponatremia and neurologic dysfunction.

Topics: Alcoholism; Demyelinating Diseases; Diuretics; Fatty Liver; Female; Humans; Hypertension; Hyponatremia; Liver Function Tests; Middle Aged; Pons; Sodium; Vasopressins

Topics: Alcoholism; Angiography; Autopsy; Esophageal and Gastric Varices; Fatty Liver; Gastrointestinal Hemorrhage; Humans; Hypertension, Portal; Infarction; Injections, Intra-Arterial; Intestine, Small; Liver Cirrhosis; Male; Mesenteric Arteries; Mesenteric Vascular Occlusion; Mesenteric Veins; Thrombosis; Vasopressins