[Diabetic diet: wholesome food in accurately adjusted portions].
Explore the source record for details and available documents.
SEARCH · PubMed Health
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
1. Rats were given low-fat diets for 3 d in which the carbohydrate source was starch. The livers of animals given the fructose or sucrose had increased hepatic activities of the fatty acid synthetase and stearoyl CoA desaturase (EC 1.14.99.5) enzyme complexes: in those given fructose there was a lower activity of the enzymes in adipose tissue. 2. Similar results were obtained in rats given fructose diets for 30 d, but in animals which had previously been made diabetic with streptozotocin, the activities were lower. The dietary treatment made little difference to the fatty acid profiles of the tissue lipids. The diabetic condition on the other hand produced considerable changes in fatty acid profile. 3. With diets containing approximately 200 g fat/kg in the form of butter or of polyunsaturated margarine, the tissue lipids from rats given sucrose had less linoleic acid than those from rats given starch. In addition, there was the expected difference between the rats given butter or margarine. The results are discussed in relation to the current literature.
AIM: Our study aims to identify novel non-coding RNA-mRNA regulatory networks associated with β-cell dysfunction and compensatory responses in obesity-related diabetes. METHODS: Glucose metabolism, islet architecture and secretion, and insulin sensitivity were characterized in C57BL/6J mice fed on a 60% high-fat diet (HFD) or control for 24 weeks. Islets were isolated for whole transcriptome sequencing to identify differentially expressed (DE) mRNAs, miRNAs, IncRNAs, and circRNAs. Regulatory networks involving miRNA-mRNA, lncRNA-mRNA, and lncRNA-miRNA-mRNA were constructed and functions were assessed through Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. RESULTS: Despite compensatory hyperinsulinemia and a significant increase in β-cell mass with a slow rate of proliferation, HFD mice exhibited impaired glucose tolerance. In isolated islets, insulin secretion in response to glucose and palmitic acid deteriorated after 24 weeks of HFD. Whole transcriptomic sequencing identified a total of 1324 DE mRNAs, 14 DE miRNAs, 179 DE lncRNAs, and 680 DE circRNAs. Our transcriptomic dataset unveiled several core regulatory axes involved in the impaired insulin secretion in HFD mice, such as miR-6948-5p/Cacna1c, miR-6964-3p/Cacna1b, miR-3572-5p/Hk2, miR-3572-5p/Cckar and miR-677-5p/Camk2d. Additionally, proliferative and apoptotic targets, including miR-216a-3p/FKBP5, miR-670-3p/Foxo3, miR-677-5p/RIPK1, miR-802-3p/Smad2 and ENSMUST00000176781/Caspase9 possibly contribute to the increased β-cell mass in HFD islets. Furthermore, competing endogenous RNAs (ceRNA) regulatory network involving 7 DE miRNAs, 15 DE lncRNAs and 38 DE mRNAs might also participate in the development of HFD-induced diabetes. CONCLUSIONS: The comprehensive whole transcriptomic sequencing revealed novel non-coding RNA-mRNA regulatory networks associated with impaired insulin secretion and increased β-cell mass in obesity-related diabetes.
A significantly lower vitamin C concentration has been found in the blood and particularly in the leukocytes of hypercholesterolemic diabetic patients than of healthy blood donors. Ascorbic acid administered in a dose of 500 mg per day for 12 months to metabolically stabilized hypercholesterolemic subjects with maturity-onset diabetes mellitus (diabetic diet without insulin or diabetic drugs) brought about a striking decline of cholesterolemia and a moderate decline of triglyceridemia. The serum lipid level in the control group given placebo remained unaltered. A daily administration of 500 mg of ascorbic acid for six months failed to affect the fasting level of serum immunoreactive insulin. It is assumed that the long-term administration of ascorbic acid to maturity-onset diabetics removed the tissue ascorbate deficiency and improved the liver ability to compensate the increased endogenous synthesis of cholesterol by its enhanced transformation to bile acids.
Explore the source record for details and available documents.
The influence of diclofenac sodium (Voltaren) on glucose metabolism was investigated in a group of 13 maturity onset diabetics treated by a standard diet alone. A second group of 14 patients with maturity onset diabetes well controlled by a standard diet and tolbutamide (Rastinon) was examined for a possible drug interaction. Determinations of capillary blood glucose as well as assessments of urine sugar by Clinitest and 24-hour urine glucose determinations were regularly done before and during treatment with diclofenac sodium. The results of this study show no alteration of glucose metabolism. These laboratory data suggest that there is no clinically relevant interaction between diclofenac sodium and tolbutamide. Neither the blood glucose profiles of the individual patients nor those of the two above-mentioned groups showed any alterations of blood glucose concentration. Diclofenac sodium, a non-steroidal antirheumatic drug, may be recommended in the treatment of rheumatic diseases in diabetics. Indomethacin, naproxen, sulindac, diftalon and diclofenac are more recently developed antirheumatic drugs which have been specially tested in diabetics.
Explore the source record for details and available documents.
The nutritional knowledge and control of diabetes was assessed in 43 nonketosis-prone diabetic subjects. Patients were semiliterate or illiterate. They were exposed to a 1-h nutritional counseling program in groups of three to five. The nutritional counseling program was highly simplified and emphasized only a few important aspects of diabetic diet. Patients' nutritional knowledge improved significantly after nutritional counseling. The control of diabetes also improved significantly in those patients in whom control had been inadequate.
Explore the source record for details and available documents.
Coincidence of chronic renal failure and diabetes mellitus brings with it serious therapeutic problems, especially in dietetic treatment. It is not possible to wish to do justice to all the therapeutic principles of the text books to the same extent. The condition of renal failure with its demands takes precedence in all cases. But if the renal disease has not yet led to a perceptible retention of normal urinary constituents in the serum, no specific dietary measures are necessary. In these cases, the diabetic diet is proceded with in the usual manner.
In a double-blind crossover study the symptomatic and metabolic effects of propranolol, acebutolol, and atenolol were studied during insulin-induced hypoglycaemia in diabetics treated with diet or hypoglycaemic tablets. All the drugs prevented tachycardia, but did not affect the other symptoms of hypoglycaemia. Propranolol delayed the recovery of the blood glucose concentration and impaired the secondary rise in the concentrations of blood lactate and non-esterified fatty acids in diet-treated diabetics. Acebutolol potentiated the hypoglycaemic effect of insulin in tablet-treated diabetics (mean difference of blood glucose concentration 0.7 mmol/l (12.6 mg/100 ml)) and this difference was maintained during the recovery phase4 the blood lactate response was also impaired. Atenolol did not differ perceptibly from placebo in its effect on the metabolic responses to acute hypoglycaemia. The results may be explained by differences in the known pharmacological actions of these drugs. They support the hypothesis that beta-adrenoreceptor blocking drugs that are highly beta1 specific and without membrane-stabilising activity should be safer than the non-selective drugs when used in diabetic patients at risk from hypoglycaemia.
Oxyhemoglobin dissociation curves (ODC) from zero to full saturation were developed from tests performed on whole blood from various groups of diabetic and nondiabetic healthy subjects. P50 at in-vivo pH was slightly but significantly lower than normal in ambulatory nonacidotic, uncomplicated juvenile diabetics (26.0 vs. 27.3 mm. Hg, P less than 0.001), despite increased red cell 2,3-diphosphoglycerate (2,3-DPG) concentrations in diabetic erythrocytes (15.0 vs. 13.7 mumole/gm. Hb, P less than 0.001). This combination of changes is in keeping with the presence of increased proportions of hemoglobin AIc in insulin-treated diabetics. The position of the ODC was positively correlated with the 2,3-DPG concentration (P less than 0.01), which varied in response to fluctuations in plasma concentration of inorganic phosphate (Pi) (P less than 0.001). Optimal metabolic control may lead to a normalization of the ODC in association with increased concentrations of red cell 2,3-DPG and P. When the diabetes was uncontrolled, the ODC was usually unchanged during the acidotic phase because the lowered pH balanced the effect of diminished 2,3-DPG concentration on the ODC. After correction of acidosis, the disproportion between erythrocyte 2,3-DPG and pH became quite prominent, accompanied by a corresponding fall in P50 (21.0 vs. 26.1 mm. Hg, P less than 0.001). Following ketoacidosis, with a persistently lowered Pi, it may take up to one week for 2,3-DPG to return to an approximately normal level, and the P50 will be impaired for the same period. A diphosphonate (EHDP) known to enhance tubular phosphate reabsorption in man was given to nonacidotic insulin-treated diabetic and healthy volunteers for 28 days. It caused a significant increase in mean Pi and P50 in both healthy and diabetic subjects (r = 0.58, P less than 0.01). When a dietary supplement of dibasic calcium phosphate was given to diabetic subjects for 28 days, a significant increase in P50 also occurred (25.2 vs. 27.2 mm. Hg, P less than 0.001). It is recommended that the diabetes diet be supplemented by dibasic calcium phosphate to prevent the inhibitory effect of a low concentration of Pi on red cell oxygen delivery.
A woman, aged 46 years, with a hyperlipoproteinemia phenotype V, an unusual type of xanthomatosis, as well as lipemia retinalis, diabetes mellitus, and nephropathia, is discussed. The withdrawal of 64 IU insulin and the institution of a hypocaloric diabetes diet resulted in the disappearance of the skin lesions and a regression of the eye lesion. During this treatment the total lipid-level became almost normal (6,965 mg% before treatment and 947 mg% after 10 weeks). The chylomicrons disappeared but the VLDL content remained relatively and absolutely elevated, as in type IV hyperlipoproteinemia.
1 In a single-blind, cross-over study fenfluramine in a daily dose of 120 mg was found to reduce the daily blood glucose level moderately in hospitalized obese diabetics treated with a 1200 calorie diabetic diet. 2 After 7 days of treatment, fenfluramine was found not to influence the intravenous glucose tolerance, the insulin response to intravenously administered glucose, or the growth hormone response to arginine. 3 No changes in blood levels of lactate, beta hydroxybutyrate, triglycerides or cholesterol were seen during fenfluramine treatment.
Nonnutritive sweeteners have been utilized in the diet of diabetic patients an an agent to replace glucose and sucrose. Since saccharin might be removed from the marketplace, the nutritive sweeteners fructose, xylitol, and sorbitol are being considered as possible alternatives for glucose and sucrose. This review considers the effects of these nutritive sweeteners on the main dietary concerns in the diabetic diet--control of blood glucose levels, obesity, and hyperlipidemia. The potential side effects of these agents are also reviewed.