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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The isolated perfused rat lung was used as a model to study the possible hormonal regulation of lipid metabolism in the mammalian adult lung. Experimental diabetes, whether induced by alloxan or streptozotocin, decreased the incorporation of [U-14C]glucose into neutral lipids and phospholipids of both the surfactant fraction and the residual fraction of the lung by 60-80%. Glucose incorporation into phosphatidylcholine and phosphatidylglycerol is decreased in experimental diabetes in both the surfactant and residual fractions to a comparable degree. Glucose incorporation is decreased in both the fatty acid and the glycerophosphocholine moieties of phosphatidylcholine isolated from the surfactant and residual fractions. Insulin treatment of normal animals 30 or 15 min prior to perfusion resulted in an approximate doubling of the incorporation of glucose into the phosphatidylcholine and phosphatidylglycerol isolated from the surfactant and residual fractions of the lung. The incorporation of glucose into palmitic acid isolated from phosphatidylcholine was also shown to increase similarly. The results of these investigations indicate that insulin may play a role in regulating the synthesis of the important lipid components of the mammalian pulmonary surfactant complex.
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PMID:Effect of experimental diabetes and insulin on lipid metabolism in the isolated perfused rat lung. 14 18

Turnover rates of glucose and free fatty acids were measured, using 3H-glucose and 14C-l-palmitic acid as tracers, in insulin-requiring diabetic patients at presentation and after insulin treatment. Correlations were sought with rates of substrate oxidation, determined independently from respiratory exchange, and with plasma hormone concentrations. The rates of appearance of glucose and of free fatty acids were increased in the diabetics to 17.6 and 10.2 micronmol min-1 kg-1 respectively. Both rates fell to normal (13.3 and 7.1 micronmol min-1 kg-1) after insulin. In the untreated state there was an inverse relationship between the rates of utilisation of glucose and free fatty acids (r = 0.61; p less than 0.05). It is suggested that this relationship represents the impairment of peripheral glucose utilisation by free fatty acids and by ketone bodies in vivo, so far only demonstrated in vitro. The tracer calculated rates of glucose utilisation correlated well over a wide range with the respiratory quotient in untreated diabetics, while respiratory quotient was inversely related to free fatty acid turnover rates. In untreated diabetics plasma cortisol and 3,3', 5'-triiodothyronine (rT3) were increased whereas thyroxine and 3,5,3'-triiodothyronine (T3) were decreased. 3,5,3'-Triiodothyronine concentration was closely related to the metabolic clearance rate of glucose (p less than 0.05), while cortisol concentrations correlated with glucose production (p less than 0.02) and blood ketone body concentration (p less than 0.02). It is concluded that glucose overproduction is the major contributor to the hyperglycaemia of untreated diabetes.
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PMID:Glucose and free fatty acid turnover in normal subjects and in diabetic patients before and after insulin treatment. 45 73

The lecithin/sphingomyelin (L/S) ratio, palmitic acid concentration and palmitic to stearic acid (P/S) ratio were estimated on samples of amniotic fluid obtained from 66 patients with diabetes. These were compared with similar estimates on amniotic fluid obtained from 127 non-diabetic patients. At 35 to 40 weeks, significant differences were observed between the L/S ratio and palmitic acid concentration in diabetics and non-diabetics, whereas the P/S ratio was similar in the two groups. The amniotic fluid L/S ratio, palmitic acid concentration, and P/S ratio were estimated on amniotic fluid obtained from 20 diabetic patients within 48 hours of induction, and the clinical outcome of the newborn infant was used to assess the predictive value of the three parameters. In 19 out of 20 diabetics the P/S ratio correctly predicted fetal lung maturity, whereas the palmitic acid concentration was correct in 12 patients and the L/S ratio in only 10 patients.
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PMID:Amniotic fluid palmitic acid/stearic acid ratios. Lecithin/sphingomyelin ratios and palmitic acid concentrations in the assessment of fetal lung maturity in diabetic pregnancies. 52 54

The fatty acid composition of total lipid and phospholipid contents was determined in the amniotic fluid of normal and diabetic pregnant patients. Disturbance of lipid metabolism which is not related to the severity of diabetes, causes difficulties in the determination of L/S ratio. The palmitic acid content of total lipid and lecithin is increased in diabetic pregnancy. The lecithin synthesis is significantly decreased as result of a transitory or prolonged acidosis.
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PMID:Palmitic acid concentration of amniotic fluid in diabetic pregnancy. 57

Palmitic acid levels were measured in samples of amniotic fluid obtained from 15 patients with diabetes. Seven patients had palmitate values which decreased at some time in pregnancy but only one of the infants developed respiratory distress. Eight of the 15 patients had final amniotic fluid palmitate values which were greater than 0.07 mmol/l and one infant developed respiratory distress. The other seven patients had final amniotic fluid palmitate values of 0.07 mmol/l or less and one of the infants developed respiratory distress. The significance of falling amniotic fluid palmitate values is discussed.
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PMID:Falling amniotic fluid palmitates in diabetic pregnancies. 58 92

A method for rapid determination of total esterified palmitic acid concentration (TEPAC) in amniotic fluid is described. The correlation coefficient between the TEPAC and the lecithin concentration was 0.93 in 123 samples of amniotic fluid obtained during the last trimester. The respiratory distress syndrome (RDS) occurred in 73% of the cases studied with TEPAC less than mmol/l in predelivery samples. The RDS was not observed with higher concentrations except in cases of maternal diabetes mellitus. The predictive value of total esterified fatty acid studies was confirmed to the concentration of palmitic acid recorded, and no specific fatty acid distributions or ratios were reliable in identifying RDS or estimating gestational age.
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PMID:Amniotic fluid palmitic acid concentrations and prediction of fetal lung maturity. 101 81

Previous assays for nonenzymatic advanced glycosylation end products (AGEs) formed in tissues and/or circulating in blood are unsatisfactory. Based on our earlier identification of AGE-specific receptors on the macrophagelike tumor cell line RAW 264.7, a new assay system for AGEs has been devised. RAW 264.7 cells were used in competitive radioreceptor assays (RRA) after a 3-day culture in 96-well plates with 1 mu CI/ml [3H]glycine. Bovine serum albumin (BSA), modified extensively by incubation with glucose-6-phosphate in vitro to form AGE-BSA, was labeled with 125I and was used as a model ligand at a concn of 10 micrograms/ml. One unit of AGE was defined as the amount of test protein required to inhibit 50% of the specific binding of [125I]-labeled AGE-BSA to the AGE-receptors of intact RAW 264.7 cells. Nonlabeled AGE-BSA was used as a specific competitor to construct standard curves. The reproducibility of the assay was assessed at AGE levels equivalent to mean, maximum, and minimum levels of sensitivity for assays run on a single day and over an extended period, and the RRA had a reproducibility (coefficient of variation) between 5.9 and 14.7%. Protease hydrolysis of in vitro glycosylated proteins before assay increases the competitive ability of these proteins in proportion to their glycosylation. Little or no AGE cross-reactivity was detected in native BSA, Amadori-BSA, maleylated BSA, formaldehyde-treated BSA, palmitic acid-BSA, and acetylated low-density lipoproteins (acetyl-LDL). Polyanions such as heparin or fucoidan strongly interfere with this receptor binding assay.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1991 Dec
PMID:Radioreceptor assay for advanced glycosylation end products. 166 95

Diabetic individuals frequently have platelet hyperaggregability and increased thromboxane (TXB2) production. To evaluate whether improvement of metabolic control or changes in fatty acid composition of serum lipids might alter thromboxane (TXB2) formation and platelet function, we followed up 25 newly diagnosed type 2 diabetics without angiopathy for about 6 months. Improvement of metabolic control (HbA1, fell from 12.0 +/- 0.3 to 9.0 +/- 0.3%; p less than 0.01) was associated with significant decrease in total cholesterol, triglycerides, and ratios of total cholesterol/HDL-cholesterol and LDL-cholesterol/HDL-cholesterol. Palmitic acid of phospholipids decreased significantly, whereas eicosapentaenoic acid increased. Regardless of this, the ADP-induced platelet aggregability and sensitivity were not altered. There was no effect whatever on the TXB2 synthesis capacity of clotting whole blood (204.9 +/- 25.0 vs 222.8 +/- 32.0 ng/ml) over 6 months of treatment. Platelet aggregability and TXB2 formation were not correlated to the degree of metabolic control, nor were there any correlations to serum lipids and their fatty acid composition. Thus, we are tempted to speculate that glucose metabolism in diabetes itself does not affect platelet aggregation or TXB2 formation in type 2 diabetes mellitus.
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PMID:Thromboxane production and platelet aggregation in type 2 diabetes mellitus without vascular complications. 174 4

Alterations in myocardial energy substrate utilization contribute to the development of cardiomyopathic changes in insulin-dependent and non-insulin-dependent diabetic rats. Energy substrate utilization and contractile function, however, have not been characterized in insulin-resistant diabetes. In this study, we studied these parameters in the insulin-resistant obese JCR:LA-cp rat homozygous for the corpulent gene (cp/cp). Homozygous (+/+) or heterozygous (+/cp) lean non-insulin-resistant rats were used as controls. Isolated working hearts from cp/cp and lean control rats were perfused with Krebs-Henseleit buffer containing either 11 mM [U-14C]glucose and 0.4 mM palmitate or 11 mM glucose and 0.4 mM [1-14C]palmitate. Unlike control hearts, hearts from cp/cp rats were found to require high doses of insulin and Ca2+ concentrations of less than or equal to 1.75 mM to maintain mechanical function. In the presence of 2,000 microU/ml insulin, contractile function from cp/cp rat hearts was not depressed in the presence of either 1.25 or 1.75 mM Ca2+. Steady-state glucose oxidation rates in hearts perfused with 1.25 mM Ca2+ and 2,000 microU/ml insulin were 811 +/- 86 (SE) and 612 +/- 51 nmol.min-1.g dry wt-1 in cp/cp and control rats, respectively. Palmitate oxidation was 307 +/- 47 and 307 +/- 47 nmol.min-1.g dry wt-1 in cp/cp and lean control hearts, respectively. Under these perfusion conditions, 40% of myocardial ATP production was derived from glucose, whereas 60% was derived from palmitate in both cp/cp and control rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Myocardial function and energy substrate metabolism in the insulin-resistant JCR:LA corpulent rat. 175 53

Altered transfer of nutrients from mother to conceptus may be involved in the pathogenesis of the developmental disturbances in offspring of diabetic mothers. In our study, the embryonic uptake of a saturated (palmitic acid) and a nonsaturated (arachidonic acid) fatty acid was evaluated in a normal and a diabetes-like environment under in vivo and in vitro conditions that yield growth retardation and somatic malformations in the embryos. The palmitic acid uptake in embryos from diabetic rats and in embryos cultured in vitro in 30 mmol/L D-glucose did not differ from the respective controls. Only embryos cultured in the highest D-glucose concentration (60 mmol/L) showed slightly increased uptake, which suggests that alterations in palmitic acid transfer have no role in the processes of embryonic maldevelopment in diabetic pregnancy. In contrast, the results showed that a diabetes-like environment both in vivo and in vitro causes increased embryonic uptake of arachidonic acid. Consequently, if the teratogenic mechanisms of diabetic pregnancy involve decreased embryonic levels of arachidonic acid, as has been suggested, this would not be the effect of a decreased uptake per se, but rather of an altered intracellular metabolism or decreased extracellular availability of this fatty acid.
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PMID:Effects of maternal diabetes or in vitro hyperglycemia on uptake of palmitic and arachidonic acid by rat embryos. 191 Jan 60


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