vitamin-b-12 and Hyperglycemia

We herein report the case of a 66-year-old Japanese man with acute-onset type 1 diabetes mellitus (T1D) accompanied by pernicious anemia. After 2 weeks of polyuria, the patient developed insulin-deficient hyperglycemia with diabetic ketoacidosis in the absence of verifiable islet-related autoantibodies and began insulin therapy in 2001. Eight years later, he developed gastric autoantibody-positive pernicious anemia and began methylcobalamin treatment. Previous studies have reported cases of slowly progressive autoimmune T1D concomitant with pernicious anemia. The present case suggests that potential associations with organ-specific autoimmune disorders should be considered during the long-term follow-up of T1D patients, even though verifiable islet-related autoantibodies are undetectable.

Topics: Aged; Anemia, Pernicious; Asian People; Autoantibodies; Diabetes Mellitus, Type 1; Diabetic Ketoacidosis; Humans; Hyperglycemia; Male; Stomach; Vitamin B 12

Topics: Biomarkers; Cobalt; Environmental Exposure; Feeding and Eating Disorders; Humans; Hyperglycemia; Joint Prosthesis; Mass Spectrometry; Polycythemia; Reference Values; Specimen Handling; Spectrophotometry, Atomic; Vitamin B 12

Topics: Adult; Animals; Biliary Tract Diseases; Child; Diabetes Mellitus; Female; Humans; Hyperglycemia; Intracranial Pressure; Liver Diseases; Pregnancy; Prenatal Care; Rats; Sorbitol; Vitamin B 12

Emerging evidence suggests that deficiencies of folate-related B vitamins can arise with metformin treatment and are independently linked with cognitive dysfunction, a comorbidity of diabetes.. To determine the impact of hyperglycemia and metformin use on relevant B vitamin biomarkers and cognitive outcomes in older adults.. Community-dwelling older adults (74.1 ± 8.3 years, n = 4160) without dementia, recruited to the Trinity, Ulster and Department of Agriculture cohort study in 2008 to 2012, were classified as normoglycemic (n = 1856) or hyperglycemic, based on HbA1c ≥5.7% (39 mmol/mol), either with (n = 318) or without (n = 1986) metformin treatment.. Biomarkers of folate, vitamin B12, vitamin B6, and riboflavin were measured. Cognitive assessments included the Repeatable Battery for Assessment of Neuropsychological Status (RBANS) and the Frontal Assessment Battery (FAB).. Metformin use was associated with higher risk of deficiency of vitamin B12 (combined B12 index ≤-1; OR 1.45; 95% CI, 1.03 to 2.02) and vitamin B6 (plasma pyridoxal 5-phosphate <30.0 nmol/L; OR 1.48; 95% CI, 1.02 to 2.15). Fortified foods when eaten regularly had a positive impact on all relevant B vitamin biomarkers, even with hyperglycemia. After adjustment for relevant covariates, metformin use was associated with an increased risk of cognitive dysfunction as assessed with the RBANS (OR 1.36; 95% CI, 1.03 to 1.80) and FAB (OR 1.34; 95% CI, 1.03 to 1.74).. Use of metformin by older adults is associated with poorer cognitive performance; B vitamin deficiency may be implicated. Fortified foods can optimize B vitamin status and may be beneficial for maintaining better cognitive health in older people with or at risk for diabetes.

Topics: Aged; Aged, 80 and over; Cognitive Dysfunction; Cohort Studies; Female; Folic Acid; Geriatric Assessment; Humans; Hyperglycemia; Independent Living; Male; Metformin; Risk Factors; Vitamin B 12; Vitamin B 12 Deficiency; Vitamin B 6

We have demonstrated previously that severe but not moderate vitamin B12 deficiency altered body composition and induced adiposity in female C57BL/6 mice. This study aims to elucidate the effects of chronic transgenerational dietary vitamin B12 restriction on body composition and various biochemical parameters in the F1 generation offspring of our mouse models of severe and moderate vitamin B12 deficiency established earlier. Female weanling C57BL/6 mice received, ad libitum, for 4 weeks a (i) control diet, (ii) vitamin B12-restricted diet with pectin as dietary fiber (severely deficient diet), or (iii) vitamin B12-restricted diet with cellulose as dietary fiber (moderately deficient diet) and then mated with control males. The offspring of control and severely deficient dams continued on the respective diets of their mothers. Few moderately deficient dams were rehabilitated to control diet from parturition and their pups were weaned to control diet. Also, some offspring born to moderately B12 deficient dams were weaned to control diet, while others continued on the same diet as their mothers. Various parameters were determined in the F1 offspring after 12 and 36 weeks of feeding. The results indicate that both severe and moderate maternal vitamin B12 restrictions were associated with accelerated catch-up growth, increased body fat percentage, visceral adiposity, dyslipidemia, fasting hyperglycemia and insulin resistance in the F1 offspring. Inflammation, increased glucocorticoid and oxidative stress and poor antioxidant defence probably underlie these adverse effects. Rehabilitation from parturition but not weaning was beneficial in delaying the onset of the adverse outcomes in the offspring. © 2016 BioFactors, 43(3):400-414, 2017.

Topics: Adipose Tissue; Animals; Blood Glucose; Body Composition; Diet; Dietary Fiber; Dyslipidemias; Female; Hyperglycemia; Inheritance Patterns; Insulin; Insulin Resistance; Male; Mice; Mice, Inbred C57BL; Obesity; Oxidative Stress; Pregnancy; Prenatal Exposure Delayed Effects; Severity of Illness Index; Vitamin B 12; Vitamin B 12 Deficiency

We investigated the preventive efficacy of exogenous methylcobalamin on sciatic nerve IGF-1 expression down-regulation and peripheral nerve deficit under different conditions (hyperglycemia and duration) of experimental diabetes in rats. Hyperglycemia was induced with streptozotocin, and stratified by exogenous insulin into mild and severe conditions. Duration of diabetes was ranged from 2-12 weeks. A single dose of methylcobalamin was intramuscularly administrated. Three groups of rats were compared in this study: (i) control group (NC, n = 30); (ii) saline-treated control diabetic group (n = 30); and (iii) methylcobalamin-treated diabetic group (n = 30). The study demonstrated a progressive decrease of sciatic nerve IGF-1 mRNA and peptide contents, and peripheral nerve dysfunction in the saline-treated diabetics over 12 weeks in contrast to the normal control non-diabetics (P < 0.01-0.0025). The IGF-1 reduction was delayed, which was consistent with retardation in nerve velocity conduction and structural impairment, in the methylcobalamin-treated diabetics, especially with mild hyperglycemia and shorter duration as compared with the saline-treated diabetics (P < 0.05-0.01). No effect of methylcobalamin on blood glucose was shown in the treated groups. It is concluded that exogenous methylcobalamin delayed onset of diabetic peripheral neuropathy via up-regulation of neural IGF-1 gene expression, and a better neuroprotective effect could be achieved in the presence of good control of hyperglycemia, especially at early stage of diabetes.

Topics: Animals; Blood Glucose; Diabetes Mellitus, Experimental; Diabetic Neuropathies; Gene Expression Regulation; Hyperglycemia; Insulin; Insulin-Like Growth Factor I; Male; Nerve Tissue Proteins; Neural Conduction; Neuroprotective Agents; Rats; Rats, Sprague-Dawley; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger; Sciatic Nerve; Severity of Illness Index; Time Factors; Up-Regulation; Vitamin B 12

Topics: Alprostadil; Anticonvulsants; Antidepressive Agents, Tricyclic; Child; Diabetic Neuropathies; Female; Humans; Hyperglycemia; Male; Mexiletine; Pain; Pain Management; Polymers; Sensation; Sodium-Potassium-Exchanging ATPase; Vitamin B 12

Topics: Acidosis; Ascorbic Acid; Blood; Cholesterol; Gastrointestinal Diseases; Glycosuria; Humans; Hydrogen-Ion Concentration; Hyperglycemia; Kidney Calculi; Oxalates; Prothrombin; Vitamin B 12

Topics: Animals; Corrinoids; Diabetes Mellitus; Diabetes Mellitus, Experimental; Hematinics; Humans; Hyperglycemia; Vitamin B 12