Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 55-years-old man with a history of alcoholism, hypertension and obesity was diagnosed of epidermoid carcinoma of the middle third portion of the esophagus. He was treated with two cycles of cytostatics with cisplatin and 5-fluorouracil. Due to his poor general health an inability to swallow solids and liquids, he received parenteral nutrition for 20 days using a commercial formula lacking in vitamins and minerals. During distal esophagectomy we observed a tendency to hypotension and severe metabolic acidosis that was unexplained by the hemodynamic profile and that persisted throughout the first 24 hours after surgery. Once these complications were corrected, he was weaned from mechanical ventilation and the following neurological signs were observed: temporal and spacial disorientation, aphasia, ophthalmoplegia with divergent strabismus and later conduction aphasia, amnesia and confabulation. Circulation was hyperdynamic, requiring inotropics and vasoconstrictors. Korsakoff syndrome secondary to Wernicke's encephalopathy was diagnosed, and the response to thiamine treatment was favorable. Beriberi can be found in hospitalized patients and the anesthesiologist may be involved in their perioperative care. Symptoms resolve easily with vitamin B1 treatment, which is ideally provided along with other hydrosoluble vitamins. Treatment should be prompt because delay leads to greater morbiomortality.
 ...
PMID:[Beriberi after esophagectomy]. 1267 75

We report three cases of dry beriberi in adolescents who underwent gastric bypass surgery for clinically severe obesity. The key to successful treatment of this problem lies in prompt recognition and thiamine supplementation.
 ...
PMID:Beriberi after gastric bypass surgery in adolescence. 1581 74

The incidence of neurologic complications from bariatric surgery is rising with the prevalence of obesity and the increasing number of bariatric surgeries. We report a 25-year-old woman who developed subacute progressive weakness and areflexia followed by confusion, ophthalmoplegia, and nystagmus following bariatric surgery. While the differential of generalized weakness with altered mental status is broad, vitamin deficiency should be routinely suspected after bariatric surgery to prevent permanent neurological injury. Multifocal neurological dysfunction in our patient represented beriberi and Wernicke's encephalopathy related to vitamin B1 deficiency.
 ...
PMID:Dry Beriberi and Wernicke's encephalopathy following gastric lap band surgery. 2252 60

In the past, food fortification along with nutritional education and the decrease in food costs relative to income have proven successful in eliminating common nutritional deficiencies. These deficiencies such as goiter, rickets, beriberi, and pellagra have been replaced with an entirely new set of "emergent deficiencies" that were not previously considered a problem [e.g., folate and neural tube defects (NTDs)]. In addition, the different nutrition surveys in so-called affluent countries have identified "shortfalls" of nutrients specific to various age groups and/or physiological status. Complex, multiple-etiology diseases, such as atherosclerosis, diabetes, cancer, and obesity have emerged. Food fortification has proven an effective tool for tackling nutritional deficiencies in populations; but today a more reasonable approach is to use food fortification as a means to support but not replace dietary improvement strategies (i. e. nutritional education campaigns). Folic acid (FA) is a potential relevant factor in the prevention of a number of pathologies. The evidence linking FA to NTD prevention led to the introduction of public health strategies to increase folate intakes: pharmacological supplementation, mandatory or voluntary fortification of staple foods with FA, and the advice to increase the intake of folate-rich foods. It is quite contradictory to observe that, regardless of these findings, there is only limited information on food folate and FA content. Data in Food Composition Tables and Databases are scarce or incomplete. Fortification of staple foods with FA has added difficulty to this task. Globally, the decision to fortify products is left up to individual food manufacturers. Voluntary fortification is a common practice in many countries. Therefore, the "worldwide map of vitamin fortification" may be analyzed. It is important to examine if fortification today really answers to vitamin requirements at different ages and/or physiological states. The real impact of vitamin fortification on some key biomarkers is also discussed. An important question also to be addressed: how much is too much? It is becoming more evident that chronic excessive intakes may be harmful and a wide margin of safety seems to be a mandatory practice in dietary recommendations. Finally, the "risk/benefit" dilemma is also considered in the "new" FA-fortified world.
 ...
PMID:Efficacy of adding folic acid to foods. 2325 98

Obesity and eating disorders are prevailing health concerns worldwide. It is important to understand the regulation of food intake and energy metabolism. Thiamine (vitamin B1) is an essential nutrient. Thiamine deficiency (TD) can cause a number of disorders in humans, such as Beriberi and Wernicke-Korsakoff syndrome. We demonstrated here that TD caused anorexia in C57BL/6 mice. After feeding a TD diet for 16days, the mice displayed a significant decrease in food intake and an increase in resting energy expenditure (REE), which resulted in a severe weight loss. At the 22nd day, the food intake was reduced by 69% and 74% for male and female mice, respectively in TD group. The REE increased by ninefolds in TD group. The loss of body weight (17-24%) was similar between male and female animals and mainly resulted from the reduction of fat mass (49% decrease). Re-supplementation of thiamine (benfotiamine) restored animal's appetite, leading to a total recovery of body weight. The hypothalamic adenosine monophosphate-activated protein kinase (AMPK) is a critical regulator of food intake. TD inhibited the phosphorylation of AMPK in the arcuate nucleus (ARN) and paraventricular nucleus (PVN) of the hypothalamus without affecting its expression. TD-induced inhibition of AMPK phosphorylation was reversed once thiamine was re-supplemented. In contrast, TD increased AMPK phosphorylation in the skeletal muscle and upregulated the uncoupling protein (UCP)-1 in brown adipose tissues which was consistent with increased basal energy expenditure. Re-administration of thiamine stabilized AMPK phosphorylation in the skeletal muscle as well as energy expenditure. Taken together, TD may induce anorexia by inhibiting hypothalamic AMPK activity. With a simultaneous increase in energy expenditure, TD caused an overall body weight loss. The results suggest that the status of thiamine levels in the body may affect food intake and body weight.
...
PMID:Thiamine deficiency induces anorexia by inhibiting hypothalamic AMPK. 2460 45

In recent times, pediatric obesity has become widely prevalent. If first-line treatment with lifestyle modification fails, bariatric surgery may be indicated for severely obese patients. Many patients now travel abroad to get these surgeries done. Some of these patients receive inadequate postoperative care. We described a morbidly obese 17-year-old girl who had a laparoscopic sleeve gastrectomy procedure for weight loss. Due to severe nausea, she stopped her multivitamin supplementation. Within a few weeks, she developed symptoms of dry beriberi was soon followed by classic symptoms of Wernicke's encephalopathy. The prompt diagnosis was made with confirmation from serum thiamine level and brain magnetic resonance imaging. Thiamine supplementation reversed ophthalmological symptoms promptly. However, the patient needed inpatient rehabilitation for neuropathy. This case describes that thiamine deficiency can occur after restrictive bariatric surgery, despite lower risk of malnutrition in the absence of intestinal bypass procedure. This report highlights that in the presence of risk factors: dietary noncompliance, inadequate follow-up, and severe nausea with and without vomiting can precipitate the development of Wernicke's encephalopathy, even after restrictive surgery. Physicians may increasingly encounter thiamine and other nutrient deficiencies in increasing numbers due to increasing prevalence of obesity disorders and availability of bariatric surgeries. This report also emphasized the importance of identifying vague sensory symptoms in thiamine deficiency.
...
PMID:Dry beriberi preceded Wernicke's encephalopathy: Thiamine deficiency after laparoscopic sleeve gastrectomy. 2655 83

Thiamine is one of several essential cofactors for ATP generation. Its deficiency, like in beriberi and in the Wernicke-Korsakoff syndrome, has been studied for many decades. However, its mechanism of action is still not completely understood at the cellular and molecular levels. Since it acts as a coenzyme for dehydrogenases of pyruvate, branched-chain keto acids, and ketoglutarate, its nutritional privation is partly a phenocopy of inborn errors of metabolism, among them maple syrup urine disease. In the present paper, we report metabolic and genomic findings in mice deprived of thiamine. They are similar to the ones we have previously found in biotin deficiency, another ATP generation cofactor. Here we show that thiamine deficiency substantially reduced the energy state in the liver and activated the energy sensor AMP-activated kinase. With this vitamin deficiency, several metabolic parameters changed: blood glucose was diminished and serum lactate was increased, but insulin, triglycerides, and cholesterol, as well as liver glycogen, were reduced. These results indicate a severe change in the energy status of the whole organism. Our findings were associated with modified hepatic levels of the mRNAs of several carbon metabolism genes: a reduction of transcripts for liver glucokinase and fatty acid synthase and augmentation of those for carnitine palmitoyl transferase 1 and phosphoenolpyruvate carboxykinase as markers for glycolysis, fatty acid synthesis, beta-oxidation, and gluconeogenesis, respectively. Glucose tolerance was initially increased, suggesting augmented insulin sensitivity, as we had found in biotin deficiency; however, in the case of thiamine, it was diminished from the 3rd week on, when the deficient animals became undernourished, and paralleled the changes in AKT and mTOR, 2 main proteins in the insulin signaling pathway. Since many of the metabolic and gene expression effects on mice deprived of thiamine are similar to those in biotin deficiency, it may be that they result from a more general impairment of oxidative phosphorylation due to a shortage of ATP generation cofactors. These findings may be relevant to energy-related disorders, among them several inborn errors of metabolism, as well as common energy disorders like obesity, diabetes, and neurodegenerative illnesses.
 ...
PMID:Thiamine Deprivation Produces a Liver ATP Deficit and Metabolic and Genomic Effects in Mice: Findings Are Parallel to Those of Biotin Deficiency and Have Implications for Energy Disorders. 2821 79