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Biomedical subjects

D Owens

Publications and source records attributed to D Owens.

At least 145 records · Page 8Linked to original sources
PubMed1977

Studies on the kinetics of unconjugated [14C]bilirubin metabolism in normal subjects and patients with compensated cirrhosis.

1. The kinetics of unconjugated [14C]-bilirubin metabolism have been investigated and analysed in terms of a three-pool model in a group of seven normal subjects and in a group of eight cirrhotic patients who had appreciable impairment of liver cell function. 2. In the patients with cirrhosis, the plasma unconjugated bilirubin was either normal or only slightly increased but the metabolism of unconjugated bilirubin was deranged. 3. The mean volume of distribution, the mean 4 h retention, and the mean mass of the rapidly mixing pool were all significantly greater than in the normal subjects. In contrast, mean fractional clearance rate and mean estimated erythrocyte life-span were significantly less than in the normal subjects. 4. The mean functional transfer rates and fluxes from pool 1 (rapidly mixing pool--'plasma') to pool 3 ('extravascular') and vice versa were significantly greater than the corresponding values in the normal subjects. 5. The results indicate that, in patients with compensated cirrhosis, the efficiency of the liver in extracting unconjugated bilirubin from plasma against a concentration gradient is impaired, even though the liver's capacity to conjugate bilirubin may be normal. As a consequence of the increased volume of distribution, the absolute hepatic clearance of unconjugated bilirubin is relatively well maintained.

Bilirubin↗
PubMed1976

Progressive intrahepatic cholestasis of infancy and childhood. A clinicopathological study of patient surviving to the age of 18 years.

A patient who developed chronic cholestatic jaundice during the 1st year of life and eventually died of liver cell failure at the age of 18 years is described. During the terminal illness Kayser-Fleischer-like rings were observed and the serum concentrations of total copper and ceruloplasmin were elevated. At autopsy, a mixed macronodular and micronodular cirrhosis was found and cholangiography and dissection of bile ducts revealed no obstructive lesion of the biliary tract. There was no family history of hepatobiliary disease. Liver biopsies obtained at the ages of 5 and 7 years showed accumulation of bile droplets in hepatocytes, normal-appearing bile ducts, no significant fibrosis, and intact lobular architecture. Striking features of the terminal cirrhosis were the presence of Mallory bodies and a marked excess of copper in the liver (2,175 mug per g dry weight). The latter two findings, as well as the elevated serum concentrations of total copper and ceruloplasmin, may be attributable to chronic cholestasis per se. This study emphasizes the clinical and therapeutic problems posed by chronic cholestasis of unknown etiology in childhood.

Adolescent↗
PubMed1975

Metabolic responses to monocomponent human insulin infusions in normal subjects and patients with liver and endocrine disease.

Hypoglycaemic and growth hormone responses were studied at different steady-state plasma insulin concentrations during a graded infusion of monocomponent human insulin. The control group consisted of ten volunteer subjects. The other groups studied included women taking oral contraceptives and patients with obesity, thyrotoxicosis, myxoedema, acromegaly, diabetes mellitus (moderate and severe) and liver disease. The hypoglycaemic response was measured in two ways: (i) the percentage reduction in plasma glucose below basal, and (ii) the rate of fall of plasma glucose (Kg-%/min). Insulin sensitivity was greatest in the normal subjects and in the other groups decreased in the order thyrotoxicosis greater than oral contraceptive greater than obesity greater than myxoedema greater than acromegaly greater than liver disease. Insulin sensitivity was difficult to assess in the diabetic patients because basal plasma glucose concentrations were elevated. At any given insulin concentration, the diabetics metabolized approximately the same amount of glucose as the normal subjects but the fact that this rate of glucose turnover occurred at higher plasma glucose concentrations probably indicated insulin resistance. Within each group Kg at each dose level of insulin correlated with the steady state plasma insulin concentration during the same infusion period. Diminishing sensitivity to insulin was reflected in an increasing fasting plasma insulin and insulin/glucose ratio except in patients with diabetes. GH responses to insulin infusion in normal subjects reflected the pattern of fall of plasma glucose. In the diabetic patients GH secretion appeared to be related to the infusion of insulin and occurred before plasma glucose had fallen to hypoglycaemic levels. GH secretory patterns were within normal limits in women taking oral contraceptives and in seven of eleven patients with liver disease but were impaired in three of seven patients with thyrotoxicosis and four of five patients with myxoedema. Four obese patients had a markedly delayed but eventually normal GH response.

Acromegaly↗
PubMed1975

Population studies on Gilbert's syndrome.

Total serum bilirubin concentration was measured by an Autoanalyzer technique in 197 normal males and 102 normal females. The mean bilirubin concentration was significantly lower in the females than in the males. Total bilirubin concentration in the males showed a bimodal distribution with an antimode at 24 mumol/1 (1.4 mg/100ml). Individuals with bilirubin concentration above this value had unconjugated hyperbilirubinaemia and probable Gilbert's syndrome. Total bilirubin concentration in the females again showed a bimodal distribution with an antimode at 12 mumol/1 (0.7 mg/100ml). It is conceivable that females with bilirubin levels above this also have Gilbert's syndrome. This suggests that the population incidence of Gilbert's syndrome could be as high as 6% and that the sex incidence is approximately equal.

Bilirubin↗
PubMed1973

Diagnosis of Gilbert's syndrome: role of reduced caloric intake test.

Reduction in caloric intake to 400 a day for 72 hours resulted in a significant increase in the plasma bilirubin concentration in patients with Gilbert's syndrome and in normal subjects. This was due to an increase in unconjugated pigment. There was no significant increase in the bilirubin concentration in patients with liver disease or haemolytic anaemia.The increase in unconjugated bilirubin was signficantly greater in Gilbert's syndrome than in normals but only when the initial bilirubin concentration was raised. It was usually seen within 24 hours of reducing the caloric intake. An increase of 100% or more suggests that unconjugated hyperbilirubinaemia is due to Gilbert's syndrome. In the normal subjects the unconjugated bilirubin level did not exceed 1.0 mg/100 ml.The increase in unconjugated bilirubin concentration on reducing the caloric intake may be due to decreased hepatic bilirubin uridine diphosphate glucuronyl transferase activity, which was shown to be present in seven rats starved for 72 hours. The effect of a 400 calorie diet for 24 hours on the unconjugated bilirubin level may distinguish Gilbert's syndrome from other causes of unconjugated hyperbilirubinaemia.

Anemia, Hemolytic↗
PubMedDate not supplied

Abnormalities in apo B-containing lipoproteins in diabetes and atherosclerosis.

Atherosclerosis is the major cause of death in patients with diabetes. Low-density lipoprotein (LDL) being the most important cholesterol-carrying lipoprotein has been studied extensively in both diabetes and non-diabetes. This paper reviews the literature but also focuses on the precursors of LDL and in particular the postprandial apo B-containing lipoproteins. Abnormalities in the postprandial lipoproteins and alteration in chylomicron assembly and clearance are discussed and the evidence presented suggesting the importance of dysregulation of these lipoproteins in atherosclerotic progression. The relationship between chylomicron production in the intestine and hepatic release of very low-density lipoproteins (VLDL) is explored, as is the interrelationship between clearance rates of these lipoproteins. The size of LDL influences its atherogenicity. VLDL composition and size in relation to its influence on LDL is discussed. The effect of diet on the composition of lipoproteins and the relationship between fatty acid composition and clearance is reviewed. Evidence that diabetic control beneficially alters lipoprotein composition is presented suggesting how improved diabetic control may reduce atherosclerosis. The review concludes with a discussion on the effect of the apo B-containing lipoproteins and their modification through glycation and oxidation on macrophage and endothelial function.

Apolipoproteins B↗
PubMedDate not supplied

Comparison of diets high in monounsaturated versus polyunsaturated fatty acid on postprandial lipoproteins in diabetes.

BACKGROUND: Postprandial hypertriglyceridaemia is common in diabetes. Fatty acids are regulators of gene expression and may play an important role in regulatingthe postprandial lipoprotein cascade. AIM: To examine postprandial lipoprotein differences between diabetic and control subjects on polyunsaturated (linoleic) and monounsaturated (oleic) fat diets. METHODS: A randomised, crossover study. RESULTS: LDL was greater and HDL less (p < 0.05) in diabetic patients compared to controls on the linoleic acid diet. Apo E per particle was significantly lower in the diabetic patients compared to control subjects on both linoleic (p < 0.05) and oleic acid diets (p < 0.01). HDL apo E was also significantly lower in the diabetic patients compared to controls on the linoleic acid diet (p < 0.02). CONCLUSION: A change from linoleic to oleic acid diet resulted in an improvement in LDL and HDL in the diabetic patients. We suggest that the reduced apo E/particle in the diabetic patients may be an explanation for the delayed lipoprotein clearance.

Case-Control Studies↗