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R G Batey

Publications and source records attributed to R G Batey.

66 records · Page 4Linked to original sources
PubMed1980

A physiological model for hepatic metabolism of transferrin-bound iron.

Hepatic iron and transferrin uptake following intravenous injection of purified native rat transferrin has been studied in the rat. Livers were removed at varying time intervals postinjection and were fractionated by isopycnic density gradient centrifugation. Neither 59Fe or 125I (labeling transferrin) appeared in the lysosomal or mitochrondrial fractions at any stage up to 14 days. 59Fe first appears in the supernatant zone of the sucrose gradient and with increasing time postinjection passes through regions of increasing density. By 16 h 59Fe became established at a density of 1.10 g/cm3 and it was identified as ferritin. Ferritin persisted labeled with 59Fe for up to 14 days. The study suggests hepatic iron uptake does not involve endocytosis. Iron is incorporated into ferritin of increasing density. This model can be used for the study of iron metabolism in human biopsy samples.

Animals↗
PubMed1979

The mechanism of hepatic iron uptake from native and denatured transferrin and its subcellular metabolism in the liver cell.

Hepatic iron uptake and metabolism were studied by subcellular fractionation of rat liver homogenates after injection of rats with a purified preparation of either native or denatured rat transferrin labelled with 125I and 59Fe. (1) With native transferrin, hepatic 125I content was maximal 5 min after injection and then fell. Hepatic 59Fe content reached maximum by 16 h after injection and remained constant for 14 days. Neither label appeared in the mitochondrial or lysosomal fractions. 59Fe appeared first in the supernatant and, with time, was detectable as ferritin in fractions sedimented with increasingly lower g forces. (2) With denatured transferrin, hepatic content of both 125I and 59Fe reached maximum by 30 min. Both appeared initially in the lysosomal fraction. With time, they passed into the supernatant and 59Fe became incorporated into ferritin. The study suggests that hepatic iron uptake from native transferrin does not involve endocytosis. However, endocytosis of denatured transferrin does occur. After the uptake process, iron is gradually incorporated into ferritin molecules, which subsequently polymerize; there is no incorporation into other structures over 14 days.

Animals↗
PubMed1978

The role of serum ferritin in the management of idiopathic haemochromatosis.

The value of the serum ferritin assay in the management of idiopathic haemochromatosis has been examined in groups of patients at diagnosis, during venesection therapy, and following completion of therapy. At diagnosis, serum ferritin levels were elevated in all 16 patients studied, including 10 with precirrhotic disease. Venesection resulted in a gradual fall in serum ferritin which commenced shortly after the start of treatment in 5/8 patients. In 3/8 the fall was preceded by a transient rise in ferritin levels. In three patients serum ferritin fell to normal before liver iron stores had been restored to normal. After therapy serum ferritin proved unreliable in detecting early re-accumulation of hepatic iron stores. Serum ferritin does provide valuable information in patients with idiopathic haemochromatosis, particularly at diagnosis and during therapy. A normal value does not exclude iron storage disease.

Adult↗
PubMed1978

Hepatic iron clearance from serum in treated hemochromatosis.

Hepatic iron uptake from transferrin has been studied in 7 patients with treated hemochromatosis. When compared with a control group with similar serum iron and transferrin saturation the hemochromatotics had a significantly higher 4-hr iron uptake value. Uptake in the precirrhotic and cirrhotic hemochromatotics was not significantly different, suggesting the existence of a cellular abnormality of hepatic iron metabolism in this disease. The results provide an explanation for the development of siderosis in some patients with idiopathic hemochromatosis and a normal serum iron concentration.

Adult↗
PubMed1977

Study of the subcellular localization of 59Fe and iron-binding proteins in the duodenal mucosa of pregnant and nonpregnant rats.

The subcellular localization of intraduodenally administered 59Fe has been studied in control, pregnant, and nonpregnant rats absorbing iron at different rates. Binding of iron to the particulate fractions of mucosal homogenates produced by centrifugation at 500, 10,000, and 100,000 X g did not vary among groups despite significant alterations in iron transport rates. Study of the 10,000 X g supernatant fluid showed that increased iron transport in iron-deficient and day 20- to 21-pregnant rats was associated with an increase in 59Fe binding to a particulate fraction of the mucosal homogenate. Although only 10 to 15% of the total mucosal 59Fe was present in the 100,000 X g supernatant in all groups, significant differences were demonstrated, among groups in the binding of iron to the three proteins present in this supernatant fraction. The proteins have been identified as ferritin, transferrin, and a protein of lower molecular weight than transferrin. Increased iron absorption was associated with a reduction in ferritin 59Fe binding and an increase in 59Fe bound to protein 3. Conversely, reduced iron absorption, was associated with increased ferritin 59Fe content and decreased protein 3 59Fe content. By studying day-21 pregnant rats 5 and 18 hr posthysterectomy it was possible to demonstrate a 12- to 18-hr delay in the intestinal mucosal protein response to alterations in the stimulus to iron absorption.

Animals↗
PubMed1977

Role of the placenta in intestinal absorption of iron in pregnant rats.

Intestinal uptake (U) and transport (T) of a 40-mug dose of 59Fe from an isolated duodenal loop has been shown to increase from day 15 of pregnancy until term in the rat. U, 60.4 +/- 4.3%, and T, 44.0 +/- 4.6%, were significantly (P less than 0.01) higher than control values, which were 31.6 +/- 3.6% and 18.9 +/- 1.8%, respectively, and resembled those in nonpregnant iron-deficient rats. Eighteen hours before the increase in absorption there was a rapid fall in the t1/2 of 59Fe in maternal serum to 37.2 +/- 3.4 min (control, 72.1 +/- 2.4 min). Hysterectomy at day 20 to 21 of pregnancy resulted in a rise in t1/2 59Fe within 5 hr to 58.0 +/- 4.7%, followed by a fall in U and T to a degree comparable to that in rats studied 18 hr postpartum. Fetectomy had no significant effect on U, 63.8 +/- 2.7%, T, 34.7 +/- 3.4%, or t1/2 59Fe, 27.8 +/- 2.5 min, when compared with corresponding values in day 20 to 21 pregnant rats. The results indicate the importance of placental iron uptake in the control of iron absorption during the 3rd week of pregnancy.

Animals↗
PubMed1976

The isolation of Bordetella bronchiseptic from an outbreak of canine pneumonia.

This report describes an outbreak of bronchitis and bronchopneumonia among young dogs in a breeding kennel following the introduction of two pups from another area. Bordetella bronchiseptica was isolated in heavy culture from affected animals which responded well to antibacterial therapy. There was no evidence of distemper virus involvement. Important bacteriological properties of Bord. bronchiseptica are discussed particularly as they relate to its known pathogenicity in the young of several species of animal. During the outbreak reported, it was noted that only young pups were clinically affected and it is suggested that Bord. bronchiseptica may be pathogenic in a certain age-group within the canine population. This seems to require further investigation.

Animals↗
PubMedDate not supplied

Non-alcoholic steatohepatitis: impaired antipyrine metabolism and hypertriglyceridaemia may be clues to its pathogenesis.

Non-alcoholic steatohepatitis resembles alcoholic liver disease in hepatic morphology but appears to have a different natural history. We sought to assess the nature of non-alcoholic steatohepatitis by a prospective study of its clinical progression and the relationship of biochemical abnormalities to changes in serum lipids among 15 patients with this disorder. In addition, antipyrine clearance (Cl-AP), which reflects hepatic microsomal oxidative capacity, was measured serially. Although initial liver histology included micronodular cirrhosis in five cases and bridging fibrosis in another three, only one patient developed a hepatic complication during 1-10 years (median: 3.7) of follow up. This confirms the relatively benign nature of non-alcoholic steatohepatitis. Moreover, Cl-AP, which was below the normal range in 13 patients, did not change significantly during 10-40 months of follow up. However, compared with other chronic liver diseases, the reduced Cl-AP was disproportionately low relative to the uniformly normal serum albumin concentration and other indices of hepatic metabolic function. This is consistent with selective impairment of endoplasmic reticular drug oxidizing enzymes. Hyperlipidaemia was present in 11 patients. In three of these, diet-induced correction of serum triglyceride elevation was associated with reduction of hepatocellular damage as indicated by serum enzyme levels. A hypothesis that unites these and earlier findings is that release of cytokines may occur in non-alcoholic steatohepatitis and produce accumulation of free fatty acids in the liver, leading to focal necro-inflammatory lesions and the destruction or down-regulation of cytochrome P450.

Adult↗