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Biomedical subjects

C Berne

Publications and source records attributed to C Berne.

At least 181 records · Page 10Linked to original sources
PubMed1975

The metabolism of lipids in mouse pancreatic islets. The oxidation of fatty acids and ketone bodies.

The rate of oxidation of 14C-labelled fatty acids and of ketone bodies was measured in isolated pancreatic islets of obese-hyperglycaemic mice (ob/ob). The following main observations were made. 1. Octanoate, palmitate and oleate were all converted into CO2 by the pancreatic islets. Octanoate was oxidized with the highest rate followed by palmitate and oleate. 2. The rate of oxidation of 0.7 mM-palmitate was 3.1 pmol/h per mug drug weight. This was decreased by 50% in the presence of 16.7 mM-glucose. The rate of palmitate oxidation was also inhibited by 2-bromostearate. The palmitate oxidation showed a concentration-dependent increase, which was most marked between 0.25 and 1.0 mM. 3. Octanoate (5 mM) had no effect on the rate of oxidation of 3.3 mM- glucose. 4. Acetoacetate (5 mM) and D-3-hydroxybutyrate (5 mM) were oxidized at rates of 5.9 and 5.4 pmol/h per mug dry weight respectively. These rates were less than 10% of those found in kidney-cortex slices. The magnitude of the oxidation rates found for fatty acids and for ketone bodies suggest that these substrates represent important metabolic fuels for the pancreatic B-cells.

Animals↗
PubMed1975

The metabolism of lipids in mouse pancreatic islets. The biosynthesis of triacylglycerols and phospholipids.

The rate of incorporation of [U-14C]glucose and [u-14C]palmitate into the lipids of the pancreatic islets of obese-hyperglycaemic mice was examined. The following main observations were made. 1. Both glucose and palmitate were incorporated into lipids in the islets. The fraction of glucose utilized for lipid biosynthesis was calculated to be 3-6% of that oxidized at high and low glucose concentrations, whereas palmitate was about equally divided between oxidation and esterification into lipids. 2. Glucose was primarily incorporated from sn-glycerol 3-phosphate. Of the total glucose carbon incorporated, only 2-4% was recovered as fatty acids. 3. A major portion of both glucose and palmitate was incorporated into phospholipids, whereas 10-30% went into triacylglycerols, depending on the extracellular glucose concentrations. 4. An increase in the glucose concentration from 3.5 to 17 mM caused a twofold increase in the rate of glucose incorporation into triacylglycerols and a fivefold increase in the rate of incorporation into phospholipids. Similar effects were also obtained with normal mouse islets. Palmitate was also preferentially directed into phospholipids by an increased glucose concentration. 5. Islets pre-labelled with radioactive palmitate showed a decrease in triacylglycerol radioactivity when they were subsequently incubated in the absence of exogenous sources of energy. 6. Mannoheptulose inhibited the rate of glucose incorporation into phospholipids, whereas omission of Ca2+ and adrenaline left phospholipid biosynthesis unimpaired. The results suggest that pancreatic B-cells have the capacity to store and utilize energy in the form of triacylglycerols. A stimulation of the B-cells by glucose is followed by an increased rate of phospholipid biosynthesis. However, this does not seem to be directly linked to the release of secretory granules.

Animals↗
PubMed1975

The effect of fatty acids and ketone bodies on the biosynthesis of insulin in isolated pancreatic islets of obese hyperglycemic mice.

Collagenase-isolated islets from obese hyperglycemic mice were used to study the effects of fatty acids and ketone bodies on insulin biosynthesis. The biosynthetic rate was quantitated as the incorporation of 3H-leucine into proinsulin and insulin, which were separated from the crude islet homogenates with anti-insulin serum coupled to cyanogen bromide activated Sepharose 4B. Palmitate and oleate did not stimulate the incorporation into proinsulin and insulin while 16.7 mM glucose caused a nine-fold increase of 3H-leucine incorporation during a 3 h incubation as compared to the basal buffer alone. A weak stimulatory effect was seen with 5 mM octanoate. The ketone bodies had a weak stimulating effect on islet protein biosynthesis, but no preferential stimulus to the insulin biosynthesis was found.

Acetoacetates↗
PubMed1975

Nicotinamide adenine dinucleotide phosphate-converting enzymes and adenosine triphosphate citrate lyase in some tissues and organs of New Zealand obese mice with special reference to the enzyme pattern of the pancreatic islets.

In order to obtain a quantitative estimate of the capacity of the pancreatic islets for provision of cytoplasmic acetyl-coenzyme A and for the turnover of nicotinamide adenine dinucleotide phosphate and its reduced form (NADP+/NADPH), the following enzymes were assayed in islets taken from New Zealand Obese mice: adenosine triphosphate citrate lyase (EC 4.1.3.8), malate dehydrogenase (decarboxylating) (NADP+) (EC 1.1.1.40), glutathione reductase (EC 1.6.4.2) and isocitrate dehydrogenase (NADP+) (EC 1.1.1.42). In addition, the activity of isocitrate dehydrogenase (NAD+) (EC 1.1.1.41) was determined. For comparative purposes the activities in exocrine pancreas, liver, heart muscle, kidney cortex and skeletal muscle were also determined. Specimens of pancreatic islets and the other tissues were microdissected from freeze-dried sections. In comparison with the other tissues, adenosine triphosphate citrate lyase was particularly active in the islets. The NADP+/NAPH-converting enzymes had activities, which suggested a rapid turnover of the islet NADP+/NADPH pool.

ATP Citrate (pro-S)-Lyase↗
PubMed1975

Anti-insulin serum coupled to Sepharose 4B as a tool for the investigation of insulin biosynthesis in the B-cells of obese hyperglycemic mice.

The biosynthetic activity of the B-cells of obese hyperglycemic mice (obob) was measured by the incorporation of [3H]leucine into proteins in collagenase-isolated pancreatic islets. To quantitate the incorporation into proinsulin and insulin, an immune binding method was used. For this purpose, anti-insulin serum was coupled to cyanogen bromide-activated SepharoseR 4B. This turned out to be a specific and versatile technique for the measurement of newly synthesized proinsulin and insulin in the B-cells. The B-cells of obob mice appear to be well adapted to a high rate of hormone biosynthesis, since at 16.7 mM glucose 44% of [3H]leucine incorporated into TCA-precipitable proteins was bound to the insulin antibodies coupled to Sepharose 4B. The insulin biosynthetic rate was stimulated 9 times at 16.7 mM glucose, during a 3-h incubation, compared with the basal insulin biosynthesis rate.

Animals↗
PubMed1974

Cytotoxic effects of streptozotocin and N-nitrosomethylurea on the pancreatic B cells with special regard to the role of nicotinamide-adenine dinucleotide.

The effects on the pancreatic B cell of streptozotocin and its aglucone derivative N-nitrosomethylurea were investigated in obese-hyperglycaemic mice and their lean littermates. Both streptozotocin and N-nitrosomethylurea were found to be B-cytotoxic although N-nitrosomethylurea produced less islet damage. Both substances decreased the concentrations of NAD(+) in the islet cells to about 10% of the control values within 2h after injection. This NAD(+) depletion was prevented by injection of nicotinamide 10min after the administration of streptozotocin or N-nitrosomethylurea. In islets taken from animals 10min after injection of streptozotocin or N-nitrosomethylurea there was no stimulatory effect of glucose on the respiration or insulin release and the oxidation of glucose was markedly decreased. Addition of nicotinamide (10mm) to the incubated islets restored glucose stimulation of both the oxygen consumption and insulin release. It is concluded that islet NAD(+) depletion is probably important for the B-cytotoxin action of N-nitrosomethylurea and streptozotocin. The glucose residue in the streptozotocin molecule may potentiate the B-cytotoxic action of this drug in mice.

Adenosine Triphosphate↗