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

Conventional treatment for gestational diabetes mellitus increases the proportion of infants born with a low birth weight, a risk factor for cardiovascular disease and diabetes mellitus in later life. Thiamine supplementation during pregnancy may be shown to be a safe preventive measure. During pregnancy, approximately 50% of the women develop a biochemical thiamine deficiency, whereas the thiamine status falls, but remains within normal limits, in most other women. Thiamine is essential for glucose oxidation, insulin production by pancreatic beta-cells and cell growth. It is therefore likely that thiamine supplementation in pregnant women not only improves their glucose tolerance but also stimulates the intra-uterine growth, thereby preventing a low birth weight to ensue from conventional therapy which only improves glucose tolerance.
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PMID:Thiamine supplementation to prevent induction of low birth weight by conventional therapy for gestational diabetes mellitus. 1102 34

Beri-Beri is caused by vitamin B1 (thiamine) deficiency. Thiamine is essential for carbohydrate metabolism and the generation of energy. Depending on age and calorie intake, 1-1.5mg/day are required with a 50% increase during pregnancy and lactation. Fever and increased muscular activity will also increase thiamine requirements (storage in muscles is limited, and reserves are quickly depleted). The sources of thiamine are meat, the outer layer of cereal grains and pulses, nuts, and leafy vegetables. The vitamin is lost during milling and processing and during excessive cooking. Beri-beri takes 2 forms: wet beri-beri which has a high output biventricular failure with edema associated with profound peripheral vasodilation and tachycardia (this also occurs in an acute fulminating form known as shoshin beri-beri) and dry beri-beri with symptoms of peripheral neuropathy with taxia, weakness, paraesthesia, and patchy sensory loss with areflexia. In this form, foot and/or wrist drop may occur. Thiamine deficiency can also produce Wernicke-Korsakoff psychosis characterized by vomiting, horizontal nystagmus, ophthalmoplegia, memory loss, and confabulation. Wet beri-beri is a medical emergency treated by intravenous administration of thiamine for several days. 38 patients (27 men and 11 women) were identified with beri-beri in urban Banjul in the Gambia. 14 had wet beri-beri, 11 a mixed presentation, and 13 dry beri-beri. Most of the patients were disabled for many months. Risk factors were pregnancy, alcohol consumption, fever, exercise, diabetes, and dysentery. 4 of the patients died (2 were in the last trimester of pregnancy). The staple diet in urban areas of the Gambia is imported, polished white rice in a groundnut- or oil-based sauce with fish and vegetables such as peppers, onions, and tomatoes. Meat is too expensive for the urban poor, and fruit and vegetable consumption is highly seasonal and income-dependent. There is little chance that this diet will be changed for the 46% of the population who live in urban areas. It is likely that a substantial proportion of the population has subclinical thiamine deficiency and are at risk of beri-beri. Since thiamine added to imported rice will be destroyed by traditional means of cooking, adding the vitamin to wheat flour may be an appropriate public health measure.
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PMID:Beri-beri: "Endemic amongst urban Gambians". 1231 72

The streptozotocin-induced (STZ) diabetic rat experimental model of diabetes on insulin maintenance therapy exhibits dyslipidemia, mild thiamine deficiency, and increased plasma protein advanced glycation end products (AGEs). The reversal of thiamine deficiency by high-dose thiamine and S-benzoylthiamine monophosphate (benfotiamine) prevented the development of incipient nephropathy. Recently, we reported that high-dose thiamine (but not benfotiamine) countered diabetic dyslipidemia. To understand further the differences between the effects of thiamine and benfotiamine therapy, we quantified the levels of the AGEs in plasma protein. We found hydroimidazolone AGE residues derived from glyoxal and methylglyoxal, G-H1 and MG-H1, were increased 115% and 68% in STZ diabetic rats, with respect to normal controls, and were normalized by both thiamine and benfotiamine; whereas N-carboxymethyl-lysine (CML) and N-carboxyethyl-lysine (CEL) residues were increased 74% and 118% in STZ diabetic rats and were normalized by thiamine only. The lack of effect of benfotiamine on plasma CML and CEL residue concentrations suggests there may be important precursors of plasma protein CML and CEL residues other than glyoxal and methylglyoxal. These are probably lipid-derived aldehydes.
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PMID:High-dose thiamine therapy counters dyslipidemia and advanced glycation of plasma protein in streptozotocin-induced diabetic rats. 1603 5

Diabetes mellitus leads to thiamine deficiency and multiple organ damage including diabetic neuropathy. This study was designed to examine the effect of benfotiamine, a lipophilic derivative of thiamine, on streptozotocin (STZ)-induced cerebral oxidative stress. Adult male FVB mice were made diabetic with a single injection of STZ (200 mg/kg, i.p.). Fourteen days later, control and diabetic (fasting blood glucose >13.9 mM) mice received benfotiamine (100 mg/kg/day, i.p.) for 14 days. Oxidative stress and protein damage were evaluated by glutathione/glutathione disulfide (GSH/GSSG) assay and protein carbonyl formation, respectively. Pro-oxidative or pro-inflammatory factors including advanced glycation end-product (AGE), tissue factor and tumor necrosis factor-alpha (TNF-alpha) were evaluated by immunoblot analysis. Four weeks STZ treatment led to hyperglycemia, enhanced cerebral oxidative stress (reduced GSH/GSSG ratio), elevated TNF-alpha and AGE levels without changes in protein carbonyl or tissue factor. Benfotiamine alleviated diabetes-induced cerebral oxidative stress without affecting levels of AGE, protein carbonyl, tissue factor and TNF-alpha. Collectively, our results indicated benfotiamine may antagonize diabetes-induced cerebral oxidative stress through a mechanism unrelated to AGE, tissue factor and TNF-alpha.
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PMID:Benfotiamine alleviates diabetes-induced cerebral oxidative damage independent of advanced glycation end-product, tissue factor and TNF-alpha. 1626 89

Accumulation of triosephosphates arising from high cytosolic glucose concentrations in hyperglycemia is one likely or potential trigger for biochemical dysfunction leading to the development of diabetic complications. This may be prevented by disposal of excess triosephosphates via the reductive pentosephosphate pathway. This pathway is impaired in experimental and clinical diabetes by mild thiamine deficiency. The expression and activity of the thiamine-dependent enzyme, transketolase--the pacemaking enzyme of the reductive pentosephosphate pathway, is consequently decreased. Correction of thiamine deficiency in experimental diabetes by high dose therapy with thiamine and the thiamine monophosphate prodrug, Benfotiamine, restores disposal of triosephosphates by the reductive pentosephosphate pathway in hyperglycemia. This prevented multiple mechanisms of biochemical dysfunction: activation of protein kinase C, activation of the hexosamine pathway, increased glycation and oxidative stress. Consequently, the development of incipient diabetic nephropathy, neuropathy and retinopathy were prevented. Both thiamine and Benfotiamine produced other remarkable effects in experimental diabetes: marked reversals of increased diuresis and glucosuria without change in glycemic status. High dose thiamine also corrected dyslipidemia in experimental diabetes--normalizing cholesterol and triglycerides. Dysfunction of beta-cells and impaired glucose tolerance in thiamine deficiency and suggestion of a link of impaired glucose tolerance with dietary thiamine indicates that thiamine therapy may have a future role in prevention of type 2 diabetes. More immediately, given the emerging multiple benefits of thiamine repletion, even mild thiamine deficiency in diabetes should be avoided and thiamine supplementation to high dose should be considered as adjunct nutritional therapy to prevent dyslipidemia and the development of vascular complications in clinical diabetes.
Curr Diabetes Rev 2005 Aug
PMID:The potential role of thiamine (vitamin B1) in diabetic complications. 1822 Jun 5

Hemodialysis patients have an elevated genomic damage in peripheral blood lymphocytes (PBLs) and an increased cancer incidence, possibly due to accumulation of uremic toxins like advanced glycation end products (AGEs). Because the vitamin B1 prodrug benfotiamine reduces AGE levels in experimental diabetes, and dialysis patients often suffer from vitamin B1 deficiency, we conducted two consecutive studies supplementing hemodialysis patients with benfotiamine. In both studies, genomic damage was measured as micronucleus frequency of PBLs before and at three time-points after initiation of benfotiamine supplementation. AGE-associated fluorescence in plasma, and in the second study additionally, the antioxidative capacity of plasma was analyzed. Benfotiamine significantly lowered the genomic damage of PBLs in hemodialysis patients of both studies independent of changes in plasma AGE levels. The second study gave a hint to the mechanism, as the antioxidative capacity of the plasma of the treated patients clearly increased, which might ameliorate the DNA damage.
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PMID:Benfotiamine reduces genomic damage in peripheral lymphocytes of hemodialysis patients. 1850 20

Wernicke encephalopathy is caused by thiamine deficiency in the central nervous system, and is defined by the triad of confusional symptoms, ocular alterations and ataxia. Some other factors may also predispose alcoholic patients to this deficiency. We report two patients with hyperglicaemia and ketoacidosis due to diabetes mellitus decompensation and chronic alcoholism who developed Wernicke encephalopathy before their hospital admission. The outcome was successful after intravenous thiamine administration and insulinotherapy. The presence of Wernicke encephalopathy in alcoholics with diabetic ketoacidosis, suggests that metabolic decompensation is essential in the onset of the disease.
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PMID:Wernicke encephalopathy in alcoholics with diabetic ketoacidosis. 1957 57

Thiamine supplementation may prevent and reverse early-stage diabetic nephropathy. This probably occurs by correcting diabetes-linked increased clearance of thiamine, maintaining activity and expression of thiamine pyrophosphate-dependent enzymes that help counter the adverse effects of high glucose concentrations-particularly transketolase. Evidence from experimental and clinical studies suggests that metabolism and clearance of thiamine is disturbed in diabetes leading to tissue-specific thiamine deficiency in the kidney and other sites of development of vascular complications. Thiamine supplementation prevented the development of early-stage nephropathy in diabetic rats and reversed increased urinary albumin excretion in patients with type 2 diabetes and microalbuminuria in two recent clinical trials. The thiamine monophosphate prodrug, Benfotiamine, whilst preventing early-stage development of diabetic nephropathy experimentally, has failed to produce similar clinical effect. The probable explanations for this are discussed. Further definitive trials for prevention of progression of early-stage diabetic nephropathy by thiamine are now required.
Diabetes Obes Metab 2011 Jul
PMID:Emerging role of thiamine therapy for prevention and treatment of early-stage diabetic nephropathy. 2134 11

Despite the targeting of traditional risk factors for cardiovascular disease, disease burden has not been completely eliminated. Thiamine is an essential cofactor in carbohydrate metabolism and individuals with diabetes are thiamine deficient. The pathophysiology of recognised complications of thiamine deficiency is similar to that underlying atherosclerosis and the metabolic syndrome, namely oxidative stress, inflammation and endothelial dysfunction. This review examines the mechanisms by which thiamine deficiency occurs in individuals with diabetes, how this deficiency leads to hyperglycaemic-induced damage, and the effect of thiamine replacement on vascular disease, endothelial function and oxidative stress. Thiamine administration can prevent the formation of harmful by-products of glucose metabolism, reduce oxidative stress and improve endothelial function. The potential benefit of long-term replacement in those with diabetes is not yet known but may reduce cardiovascular risk and angiopathic complications.
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PMID:Thiamine deficiency in diabetes mellitus and the impact of thiamine replacement on glucose metabolism and vascular disease. 2156 42

Morbid obesity is a curable systemic disease that can cause several complications, including hypertension, diabetes mellitus, and osteoarthritis. However, it is not easy to control solely by conservative management. Bariatric surgeries, such as sleeve gastrectomy and gastric banding, are recently developed treatments that are applied to patients with morbid obesity in Korea. However, gastric surgery can cause surgical or metabolic complications, such as thiamine deficiency, which can lead to Wernicke's encephalopathy. This metabolic complication presents with typical symptoms of confusion, ophthalmoplegia, nystagmus, and ataxia. In this case report, we present a case of Wernicke's encephalopathy, which developed slowly following sleeve gastrectomy in a patient with morbid obesity.
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PMID:Wernicke's Encephalopathy after Sleeve Gastrectomy for Morbid Obesity - A Case Report -. 2250 78


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