A complex role of activin A in non-alcoholic fatty liver disease.

Objectives: Recent studies suggest that activin A, a member of the transforming growth factor (TGF) superfamily, is involved in the pathogenesis of liver disorders. We sought to explore its possible role in non-alcoholic fatty liver disease (NAFLD).

Methods: Serum levels of activin A and its natural inhibitor, follistatin, were measured in patients with NAFLD (n=70) and in control subjects (n=30).

Abnormal glucose tolerance is a predictor of steatohepatitis and fibrosis in patients with non-alcoholic fatty liver disease.

Objective: The majority of patients with non-alcoholic fatty liver disease (NAFLD) have simple steatosis. A minority, however, present with non-alcoholic steatohepatitis (NASH), a condition that can lead to advanced fibrosis and cirrhosis. The frequencies of NASH and fibrosis among patients with NAFLD and sustained elevation of liver function tests (LFT) are uncertain.

Effects of the prostaglandin E2 analogue enprostil on the carbon tetrachloride-induced necrosis of liver cells in mice.

Female mice, eight weeks old, were injected with carbon tetrachloride (CCl4) (10 mg subcutaneously). Groups of mice (n = 10-30) were then injected with enprostil (E) 2, 20 or 50 micrograms/kg body weight (bw) intraperitoneally 15 min and two h after, or E 100 micrograms/kg bw two h after the CCl4 injection. The mice were killed after 24, 48 or 72 h.

Liver cell necrosis and regeneration following injections of carbon tetrachloride. Effects of the thyrotropin-releasing hormone and somatostatin.

Mice were given 10 micrograms somatostatin or 25 micrograms TRH intraperitoneally 10 min before s.c. injection of 2 or 20 mg CCl4.

Diminution of postprandial release of pancreatic polypeptide in myotonic dystrophy.

The meal-stimulated release of pancreatic polypeptide (PP), gastrin, somatostatin and glucagon was studied in nine patients with myotonic dystrophy (MD) and in 11 healthy controls. PP-release was significantly reduced in MD compared to controls. This reduction may be related to the abnormal gut motility demonstrated in MD.

The immediate effect of human renal transplantation on basal and meal-stimulated levels of gastrointestinal hormones.

Elevated serum levels of gastrin, pancreatic polypeptide, and glucagon were found in 10 uraemic patients, whereas gastric inhibitory polypeptide and somatostatin levels were normal. After renal transplantation there was a significant reduction in serum gastrin (median, 5 pmol/l; p = 0.05, n = 9), pancreatic polypeptide (145 pmol/l; p less than 0.

Autopsy findings in three family members with a presumably acquired immunodeficiency syndrome of unknown etiology.

This paper presents clinical, immunological and post-mortem findings in three family members (husband, wife and daughter) who all died in 1976 after having had chronic and recurrent opportunistic infections for many years. In all of them a progressive, presumably acquired T-lymphocyte defect associated with B-lymphocyte dysfunction had been diagnosed several years before death. The clinical and immunological findings are compatible with those seen in acquired immunodeficiency syndrome (AIDS) caused by HTLV-III/LAV infection, but examinations of stored blood samples from the three patients were negative with regard to the presence of HTLV-III/LAV antibodies.

The antisecretory effects of RP 40 749 in patients with previous duodenal ulcer.

Thirteen male patients with a history of duodenal ulcer were given 150 mg RP 40 749 or placebo tablets at bedtime in a double-blind crossover study. The medication was given for two periods of 10 days with an 11-day wash-out period between. pH and pepsin concentrations were determined each hour in aspirates of gastric juice for 24 h on day 1, 10, 22, 31, and a 2-h collection of gastric juice was examined in the middle of the treatment and wash-out periods.

Dopaminergic and adrenergic influence on gastric acid and pepsin secretion stimulated by food. The role of vagal innervation.

Dopaminergic and adrenergic mechanisms were studied in a dog model which made possible physiological stimulation by food and comparison of vagally innervated and denervated acid and pepsin response at the same time. Five dogs were equipped with two pouches separated from the stomach, and stimulation was done by a standard meal - a mixture of liver, heart and bonemeal , 10 g/kg. The meal was combined with different doses of dopamine 0.

Pancreatic polypeptide release stimulated by food, secretin and cholecystokinin in chronic pancreatitis.

The pancreatic polypeptide (PP) release after a standard meal and the PP release and the pancreatic secretion of bicarbonate and amylase after stimulation by secretin GIH, 1 CU kg-1 intravenously, and by cholecystokinin (CCK), 1 Ivy dog unit kg-1 intravenously, have been investigated in 10 patients with chronic pancreatitis. Significant correlations were found between the integrated PP responses after food and hormonal stimulation (p less than 0.05), between the integrated PP response and the peak serum PP concentration after food (p less than 0.

The release of human pancreatic polypeptide, gastrin, gastric inhibitory polypeptide, and somatostatin in celiac disease related to the histological appearance of jejunal mucosa before and 1 year after gluten withdrawal.

Jejunal biopsies and the postprandial response of pancreatic polypeptide (PP), gastrin, gastric inhibitory polypeptide (GIP), and somatostatin have been examined in nine patients with celiac disease before and 1 year after gluten withdrawal. All presented initially with total villous atrophy of the jejunal mucosa. After gluten withdrawal five showed marked mucosal regeneration on light microscopy examination (responders) and four only moderate or no regeneration (nonresponders).

The effect of histamine, H1 and H2 agonists, and H1 and H2 antagonists on postprandial pancreatic polypeptide release in dogs.

The influence of histamine, H1 and H2 agonists (2-AETD and dimaprit), and H1 and H2 antagonists (mepyramine and cimetidine) on the postprandial release of pancreatic polypeptide (PP) was assessed in five Labrador retrievers. Infusions of histamine, 0.25 mumol kg-1 h-1; 2AETD, 4 mumol kg-1 h-1; and dimaprit, 1 mumol kg-1 h-1, enhanced postprandial release (131-189% of control values).

The effect of alpha- and beta-adrenergic agonists and blockers on postprandial pancreatic polypeptide release in dogs.

The influence of adrenergic agonists--phenylephrine (alpha), isoproterenol (beta), and salbutamol (beta 2)--and of adrenergic blockers--phentolamine (alpha), pranolol (beta), and practolol (beta 1)--on the postprandial pancreatic polypeptide (PP) release has been assessed in five Labrador retrievers. Infusions of phenylephrine, 0.12 mg kg-1h-1; isoproterenol, 3 micrograms kg-1h-1; salbutamol, 12 micrograms kg-1h-1, did not significantly affect PP release.

Effects of dopamine and dopamine antagonists on postprandial release of pancreatic polypeptide in dogs and in healthy volunteers.

The effect of dopamine, 0.006, 0.12, 1.

Effect of cholinergic and adrenergic blockade on human pancreatic polypeptide secretion in healthy subjects.

The effect of cholinergic, alpha-adrenergic, and beta-adrenergic blockade on human pancreatic polypeptide (HPP) release has been tested in six normal subjects before and after a meal. The response to food was abolished by atropine and significantly enhanced by phentolamine and propranolol. The increase induced by phentolamine occurred during the primary phase 0-60 min after food, and that caused by propranolol was observed during the secondary phase 60-120 min postprandially.