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

Complamine (xanthinol-nicotinate) injected intravenously in a dose of 300 mg caused in patients with diabetes mellitus a significant, although short-lived improvement of the indices of intrahepatic circulation (by the rheohepatographic criteria). By itself complamine failed to influence the pancreatic secretion of amylase, lipase, and trypsin, but regularly intensified the stimulating action of pancreosimine on the pancreatic secretion of the enzymes in the patients with diabetes. In addition to the known influence of complamine on the circulation in the lower limbs of the patients with diabetes mellitus, information presented in the given work widened the circle of indications to the therapeutic use of complamine in patients with diabetes mellitus with disturbances of intrahepatic hemodynamics and the enzyme-secretory insufficiency of the pancreas. Complamine should be administered after meals at the period of the greatest release of the endogenous pancreosimine, for the intensification of the pancreatic enzymes secretion.
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PMID:[Effect of Complamin on the intrahepatic blood flow and pancreatic secretion of enzymes in diabetes mellitus]. 34 35

The urinary excretion of metabolites of the tryptophan leads to niacin pathway after an L-tryptophan load in patients with potential and latent diabetes, and in a third of those with chemical diabetes, was normal. In the remaining subjects with chemical diabetes and in those with clinical diabetes it was altered and characterized by an increase of xanthurenic acid and by a reduction of kynurenines and 3-hydroxyanthranilic acid. The thin-layer chromatographic pattern of tryptophan metabolites in the epidermis of patients with potential, latent, chemical, clinical diabetes was characterized by the kynurenine pathway metabolites that were also present in the epidermis of healthy subjects. Morevoer, the above pattern was characterized by the appearance of 5-hydroxytrptamine, and in patients with chemical and clinical diabetes by the appearance of xanthurenic acid.
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PMID:Identification of tryptophan metabolites in the healthy epidermis of diabetics. 59 99

Coffee as a rule develops stimulating effects on the central nervous system, heart and circulation which are mainly caused by caffeine. In certain cases coffee may also have a sedative effect and sometimes even it is useful to fall asleep quickly. Furthermore coffee may be advantageous in the treatment of some functional disorders caused by lacking of dopamine, because coffee is able to increase the dopamine formation in brain. Concerning the effects of coffee in the gastrointestinal-tract and liver-bile system caffeine is only of secondary importance. Hereby certain roasting substances, possibly also chlorogenic acid or caffeic acid should be responsible for the stimulating effects observed in these organs. These stimulating effects could be caused whether directly or indirect e.g. by liberating gastrin or other gastrointestinal hormones. Vitamin niacin, which is formed in greater amounts from trigonelline during the roasting process, may also be important from the nutritional standpoint. Therefore coffee may be prescribed as a true drug in cases of deficiency in vitamin niacin or also in the pellagra disease. By extensive epidemiological studies performed lately it could be demonstrated that there exists no correlation between coffee consumption and certain risk factors as hypertension, heart infarction, diabetes, gout or cancer diseases. Furthermore there was no evidence that coffee or its caffeine content are able to induce genetic alterations or even malformations.
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PMID:[Coffee and health]. 60 27

North American Indians have a higher morbidity from gallbladder disease, diabetes mellitus and obesity than other North Americans; this may result from their food intake. Nutrient intake and meal patterns were compared in 120 Micmac Indian and 115 Caucasian women in Shubenacadie, NS. Findings were compared with the Canadian Dietary Standard (CDS) and the Nutrition Canada national and Indian survey reports. The diet of Indian women had higher carbohydrate, lower protein and lower fibre content than that of Caucasian women, who derived a higher percentage of energy from protein and had a higher intake of vitamin A, niacin and ascorbic acid. Overnight fast was longer among Indian women. A high percentage of all women studied reported diets that did not reach the CDS for total energy intake in kilocalories or for calcium, iron, vitamin A, thiamin or riboflavin.
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PMID:Nutrient intake and meal patterns of Micmac indian and Caucasian women in Shubenacadie, NS. 86 96

Water-soluble group B vitamins metabolism was studied over the course of streptozotocin-induced diabetes mellitus in rats fed semisynthetic isocaloric diets containing 18 and 50% of protein. A high-protein diet in diabetes mellitus does not influence riboflavin metabolism disordered in this disease but reduced 4-pyridoxyl acid excretion to the level characteristic of healthy animals. The observed trend to an increase of liver nicotinamide coenzymes levels and of 1-methylnicotinamide urinary excretion reflects increased niacin synthesis from the diet protein tryptophan, for niacin level is reduced in diabetes.
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PMID:[Effect of protein content in rat diet on water-soluble vitamin metabolism in streptozotocin-induced diabetes]. 130 52

Tocopherol has been shown to have antiplatelet effects in insulin-dependent diabetes mellitus. However, its antiplatelet effect in non-insulin-dependent diabetes mellitus (NIDDM) remains to be established. In this report, the antiplatelet effect of tocopherol was assessed in a randomized, double-blind and crossover study of 15 NIDDM subjects. Each subject received tocopherol (dl-alpha-tocopherol nicotinate, 200 mg, tid) and a placebo for two six-week treatment periods separated by a three-week period in between for wash-out. The mechanisms of the antiplatelet effect of tocopherol were also studied in vitro. A significant decrease in platelet reactivity was observed after tocopherol treatment as compared with the pretest, and the magnitude of the decrease during tocopherol treatment was significantly evident when compared with that of the placebo treatment, as assessed by collagen (5, 10 micrograms/mL)-induced platelet aggregation of whole blood. A dose-dependent reduction in both ADP-and collagen-induced platelet aggregation was observed with tocopherol from 0.1 to 3.0 mM in vitro. No corresponding changes in ATP secretion and thromboxane synthesis were observed. Tocopherol also significantly inhibited fibrinogen-induced aggregation of elastase-treated platelets at a concentration of 0.1 mM. We demonstrated that platelet aggregation of whole blood ex vivo, among 15 NIDDM subjects was suppressed in tocopherol treatment, so tocopherol may have an antiplatelet effect in NIDDM subjects. The inhibitory effect of the platelet aggregation of tocopherol may be partially accomplished through interference with fibrinogen binding towards its receptor.
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PMID:Effect of tocopherol on platelet aggregation in non-insulin-dependent diabetes mellitus: ex vivo and in vitro studies. 135 87

Hypertriglyceridemia is not a common finding in well controlled patients with insulin dependent diabetes; however, in noninsulin dependent, or Type II diabetes, hypertriglyceridemia and coronary heart disease are a well recognized clinical triad. In the latter setting, hypertriglyceridemia is usually the result of an associated inherited hyperlipidemia, most commonly familial hypertriglyceridemia but also familial combined hyperlipidemia. In the former, one sees elevated triglycerides and a low HDL-cholesterol, in the latter the same phenotype may be present but often there is a high LDL-cholesterol. Irrespective of the pathogenesis of the primary hypertriglyceridemic disorder, the occurrence of poorly controlled diabetes will enhance the hypertriglyceridemia and even in the Type II diabetic, with triglycerides in the thousands, dietary and glycemic control, alone, will strikingly ameliorate the hypertriglyceridemia. In contrast to patients with hypercholesterolemia, no national guidelines have been proposed for the treatment of patients with hypertriglyceridemia. Yet both experimental and clinical data support an algorithm in which dietary and glycemic control are optimized with a resultant major improvement in triglycerides, followed by the introduction of drug therapy. Three agents are particularly useful in correcting the hypertriglyceridemia: gemfibrozil, niacin, and fish oils, with the first two having the added benefit of increasing HDL levels. Lovastatin is also useful in treating these patients, but primarily for lowering LDL-cholesterol while triglycerides are independently being brought under control. Correction of hyperlipidemia in diabetic patients can generally be achieved with judicious use of dietary, glycemic and drug therapy; however, maintenance of a favorable response requires a high level of patient compliance, which is usually difficult to sustain.
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PMID:Hypertriglyceridemia in diabetes. An approach to management. 176 54

(1) Streptozotocin-diabetes decreased the responsiveness of noradrenaline- or forskolin-stimulated lipolysis to inhibition by phenylisopropyladenosine (PIA), prostaglandin E1 (PGE1) and nicotinate in rat adipocytes. (2) Diabetes had no effect on high affinity binding of [3H]PIA to adipocyte plasma membranes. (3) Plasma membranes from diabetic animals had increased abundance of alpha-subunits of Gi1 and Gi2. The effect of pertussis toxin in overcoming inhibition of lipolysis by PIA was delayed in adipocytes from diabetic rats. (4) Diabetes decreased the GTP-dependent right-wards shift in the dose-curve for displacement of the antagonist [3H]DPCPX by PIA in adipocyte plasma membranes. (5) It is concluded that, despite increased abundance of Gi in diabetic adipocytes, less of this is functional. This may contribute to reduced sensitivity to PIA, PGE1 and nicotinate and explains some of the loss of control of lipolysis in insulin-dependent diabetes.
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PMID:Diabetes decreases sensitivity of adipocyte lipolysis to inhibition by Gi-linked receptor agonists. 178 8

The Lens Opacities Case-Control Study evaluated risk factors for age-related nuclear, cortical, posterior subcapsular, and mixed cataracts. The 1380 participants were ophthalmology outpatients, aged 40 to 79 years, classified into the following groups: posterior subcapsular only, 72 patients; nuclear only, 137 patients; cortical only, 290 patients; mixed cataract, 446 patients; and controls, 435 patients. In polychotomous logistic regression analyses, low education increased risk (odds ratio [OR] = 1.46) and regular use of multivitamin supplements decreased risk (OR = 0.63) for all cataract types. Dietary intake of riboflavin, vitamins C, E, and carotene, which have antioxidant potential, was protective for cortical, nuclear, and mixed cataract; intake of niacin, thiamine, and iron also decreased risk. Similar results were found in analyses that combined the antioxidant vitamins (OR = 0.40) or considered the individual nutrients (OR = 0.48 to 0.56). Diabetes increased risk of posterior subcapsular, cortical, and mixed cataracts (OR = 1.56). Oral steroid therapy increased posterior subcapsular cataract risk (OR = 5.83). Females (OR = 1.51) and nonwhites (OR = 2.03) were at increased risk only for cortical cataract. Risk factors for nuclear cataract were a nonprofessional occupation (OR = 1.96), current smoking (OR = 1.68), body mass index (OR = 0.76), and occupational exposure to sunlight (OR = 0.61). Gout medications (OR = 2.48), family history (OR = 1.52), and use of eyeglasses by age 20 years, which is an indicator of myopia (OR = 1.44), increased risk of mixed cataract. The results support a role for the nutritional, medical, personal, and other factors in cataractogenesis. The potentially modifiable factors suggested by this study merit further evaluation.
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PMID:The Lens Opacities Case-Control Study. Risk factors for cataract. 184 56

A decrease in the vitamin E content of human diabetic platelets is closely associated with the accelerated platelet aggregation and platelet prostaglandin metabolism seen in patients with diabetes mellitus. We investigated the effect of vitamin E supplementation on these abnormalities of physiological function and prostaglandin metabolism in 14 non-insulin dependent diabetics with proliferative retinopathy. ADP-induced platelet aggregation was inhibited in vitro by the addition of vitamin E in a dose-dependent manner. However, in lower concentrations considered to be physiological doses in vivo, significantly greater inhibition was observed in diabetic platelets than in the control platelets. Next, alpha-tocopheryl nicotinate was administered to diabetics at a daily dose of 600 mg. The platelet vitamin E content was restored to control levels in 13 of the 14 patients after 2-4 weeks of daily administration. The ADP-induced platelet aggregation rate, platelet thromboxane B2 (TXB2, a stable metabolite of TXA2, a vasoconstrictor production, and plasma TXB2 level were low in all 14 diabetics. In contrast, plasma 6-keto-PGF 1 alpha (a stable metabolite of PGI2, a vasodilator) was significantly increased and therefore the 6-keto-PGF 1 alpha/TXB2 ratio in plasma was restored to within normal limits. These results indicate that vitamin E may improve platelet function and prostaglandin metabolism in diabetes mellitus and may be able to provide further beneficial effects in relation to the development of diabetic vascular complications.
Diabetes Res 1990 May
PMID:Effects of vitamin E administration on platelet function in diabetes mellitus. 213 64


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