Thiamine deficiency affects glucose transport and β‐oxidation in rats

Abstract

Thiamine is recognized as a cofactor for many enzymes involved in intermediary metabolism responsible for energy production. Animal model of thiamine deficiency (TD) included direct evaluation of glucose uptake by estimation of 3H‐deoxyglucose transport across red blood cells membranes and β‐oxidation of fatty acids in isolated leucocytes. Feeding of animals with the thiamine‐deficient diet (0.018 mg/kg diet) for 30 days resulted in disturbances in energy production. The thiamine intake was limited not only by vitamin B1 deficiency in the diet, but also by time‐dependent drop of feed consumption by rats fed this diet. At the end of experiment, diet consumption in this group of rats was 52% lower than in the control group. This was accompanied by low glucose uptake by erythrocytes of rats suffering vitamin B1 deficiency for longer time. At the end of experimental period, glucose uptake was over 2 times lower in TD erythrocytes than in control RBC. Such drop of energy production was not compensated by delivery of energy from fatty acid degradation. In leucocytes from TD rats, the β‐oxidation was also suppressed. Observed significant decrease of serum insulin from 2.25 ± 0.25 ng/ml (day 0) to 1.94 ± 0.17 ng/ml (day 30) might have significant impact on observed energy production disorders. The results from this study indicate that the thiamine deficiency significantly reduces feed intake and causes modest abnormalities in glucose and fatty acid utilization.

Effects of Thiamin Restriction on Exercise-Associated Glycogen Metabolism and AMPK Activation Level in Skeletal Muscle

“…The rats consumed the assigned diets ad libitum for 1 week until the end of the dark cycle (06:00) on the day of dissection. The experimental period was decided based on previous studies [ 12 , 17 , 18 , 19 ]. These studies demonstrated that no symptoms of thiamin deficiency such as anorexia, weight loss, and behavior disorders were observed on the 7th day of the intervention with thiamin-deficient diet.…”

Hiding in Plain Sight: Modern Thiamine Deficiency

“…With insufficient thiamine, TKT activity downregulates, cell proliferation, myelin synthesis, and antioxidant capacity are impaired [66] and glucose metabolism is diverted out of the PPP toward the polyol/sorbitol, hexosamine, diacylglycerol/PKC, advanced glycation end product (AGE) pathways [67]. This shift in how carbohydrates are metabolized, not only reduces substrate availability for the production of ATP, but also, becomes part of the metabolic inflexibility so commonly observed with type 2 diabetes and associated cardiovascular disease [37,68,69].…”

“…Hyperglycemia, in turn, is frequently associated with nutrient deficiency and met-abolic dysfunction affecting not just glucose handling, but fatty acid and amino acid handling as well. With hyperglycemia, the metabolism of excess sugars, those that cannot enter OXPHOS or the PPP, are diverted through the polyol/sorbitol, hexosamine, diacylglycerol/PKC, AGE pathways [67], leading to both decrements in ATP production and macro-and microvascular cell damage [69,133]. This is in addition to poor BCAA catabolism [134] with increased branched chain keto acids [80], and poor fatty acid metabolism with increased phytanic acid and disrupted sphingolipid homeostasis [81,82].…”

Dietary Micronutrient Management to Treat Mitochondrial Dysfunction in Diet-Induced Obese Mice

“…Vitamin B1 (thiamine) is recognized as a cofactor for mitochondrial enzyme complexes that is involved in intermediary metabolism responsible for energy production. Accordingly, thiamine deficiency is associated with disorders in adenosine triphosphate (ATP) production [ 16 ] and reduction in fatty acid oxidation [ 17 ]. Vitamin B1 is also a cofactor of transketolase, a cytosolic enzyme involved in the pentose phosphate pathway which plays a major role in the production of nicotinamide adenine dinucleotide phosphate-hydrogen (NADPH) for maintaining cellular redox status, glutathione (GSH) levels and protein sulphydryl groups, as well as fatty acid synthesis.…”