Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0948265 (metabolic syndrome)
 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Perinatal nutrition has persistent influences on neural development and cognition. In humans and other animals, protein malnutrition during the perinatal period causes permanent changes, inducing to adulthood metabolic syndrome. Feeding is mainly modulated by neural and hormonal inputs to the hypothalamus. Hypothalamic glycogen stores are a source of glucose in high energetic demands, as during development of neural circuits. As some hypothalamic circuits are formed during lactation, we studied the effects of malnutrition, during the first 10 days of lactation, on glycogen stores in hypothalamic nuclei involved in the control of energy metabolism. Female pregnant rats were fed ad libitum with a normal protein diet (22% protein). After delivery, each dam was kept with 6 male pups. During the first 10 days of lactation, dams from the experimental group received a protein-free diet and the control group a normoprotein diet. By post-natal day 10 (P10), glycogen stores were very high in the arcuate nucleus and median eminence of control group. Glycogen stores decreased during development. In P20 control animals, glycogen stores were lower when compared to P10 control animals. Animals submitted to malnutrition presented a staining even lower than control ones. After P45, it was difficult to determine differences between control and diet groups because glycogen stores were reduced. We also showed that tanycytes were the cells presenting glycogen stores. Our data reinforce the concept that maternal nutritional state during lactation may be critical for neurodevelopment since it resulted in a low hypothalamic glycogen store, which may be critical for establishment of neuronal circuitry.
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PMID:Glycogen stores are impaired in hypothalamic nuclei of rats malnourished during early life. 2013 51

Glycogen storage in human organism is providing reserve source of glucose which is critical for normal functioning of the nervous system during periods between meals and is also important for many other tissues. Overwhelming excessive consumption of carbohydrates and decreasing physical activity among the world population lead to dramatic increase in incidence and mortality related to cardiovascular diseases, metabolic syndrome and diabetes mellitus type 2. There is an observation that many interventions with proved clinical efficiency like physical activity, intermittent fasting, caloric restriction and some pharmacological treatments have in common the ability to decrease content of glycogen in the liver and skeletal muscles. This effect leads to increased ability of these organs to uptake the next dose of glucose and store it in the form of glycogen. Moreover these interventions lead to significant life span extension, provide better body fitness and prevent development of multiple age-related diseases. In contrast excessive glucose load and saturation of tissues with glycogen provide a metabolic shift toward synthesis of fatty acids by liver. In advanced stages decreased glucose tolerance, insulin resistance, hyperinsulinemia, fatty liver disease, impairment of liver function and derangements of cholesterol metabolism are observed. It is suggested that noninvasive measurement of glycogen content in tissues could serve as important diagnostic and follow-up parameter for clinical practice and healthy lifestyle in wide population groups.
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PMID:An intermittent exhaustion of the pool of glycogen in the human organism as a simple universal health promoting mechanism. 2449 63

The metabolic syndrome is a group of metabolic alterations considered a worldwide public health problem. Organic selenium compounds have been reported to have many different pharmacological actions, such as anti-hypercholesterolemic and anti-hyperglycemic. The aim of this study was to evaluate the effect of p-chloro-diphenyl diselenide (p-ClPhSe)2, an organic selenium compound, in a model of obesity induced by monosodium glutamate (MSG) administration in rats. The rats were treated during the first ten postnatal days with MSG and received (p-ClPhSe)2 (10 mg/kg, intragastrically) from 45th to 51 th postnatal day. Glucose, lipid and lactate levels were determined in plasma of rats. Glycogen levels and activities of tyrosine aminotransferase, hexokinase, citrate synthase and glucose-6-phosphatase (G-6-Pase) were determined in livers of rats. Renal G-6-Pase activity was also determined. The purine content [Adenosine triphosphate (ATP), adenosine diphosphate (ADP) and adenosine monophosphate] and mitochondrial functionality in the liver were also investigated. p-(ClPhSe)2 did not alter the reduction in growth performance and in the body weight caused by MSG but reduced epididymal fat deposition of rats. p-(ClPhSe)2 restored glycemia, triglycerides, cholesterol and lactate levels as well as the glucose metabolism altered in rats treated with MSG. p-(ClPhSe)2 restored hepatic mitochondrial dysfunction and the decrease in citrate synthase activity and ATP and ADP levels caused by MSG in rats. In summary, (p-ClPhSe)2 had homeostatic effects on glucose metabolism and mitochondrial function alterations induced by MSG administration to rats.
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PMID:Homeostatic effect of p-chloro-diphenyl diselenide on glucose metabolism and mitochondrial function alterations induced by monosodium glutamate administration to rats. 2629 81