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)

High fructose consumption is associated with the development of fatty liver and dyslipidemia with poorly understood mechanisms. We used a matrix-assisted laser desorption/ionization-based proteomics approach to define the molecular events that link high fructose consumption to fatty liver in hamsters. Hamsters fed high-fructose diet for 8 weeks, as opposed to regular-chow-fed controls, developed hyperinsulinemia and hyperlipidemia. High-fructose-fed hamsters exhibited fat accumulation in liver. Hamsters were killed, and liver tissues were subjected to matrix-assisted laser desorption/ionization-based proteomics. This approach identified a number of proteins whose expression levels were altered by >2-fold in response to high fructose feeding. These proteins fall into 5 different categories including (1) functions in fatty acid metabolism such as fatty acid binding protein and carbamoyl-phosphate synthase; (2) proteins in cholesterol and triglyceride metabolism such as apolipoprotein A-1 and protein disulfide isomerase; (3) molecular chaperones such as GroEL, peroxiredoxin 2, and heat shock protein 70, whose functions are important for protein folding and antioxidation; (4) enzymes in fructose catabolism such as fructose-1,6-bisphosphatase and glycerol kinase; and (5) proteins with housekeeping functions such as albumin. These data provide insight into the molecular basis linking fructose-induced metabolic shift to the development of metabolic syndrome characterized by hepatic steatosis and dyslipidemia.
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PMID:Proteomic analysis of fructose-induced fatty liver in hamsters. 1864 Mar 90

Identification and characterization of novel genes involved in derangement of metabolisms of glucose and triglycerides are important in understanding the development of metabolic syndrome (MS) and atherosclerosis. Model rats with certain phenotypes of MS were fed a high-carbohydrate diet. The rat hepatic subtracted cDNA libraries were constructed and screened. A novel cDNA of full length was identified by screening of a human hepatic cDNA library with a mixture of probes of the differentially expressed fragments from the rat hepatic subtracted cDNA libraries. The corresponding gene of the cDNA was temporarily named metabolic syndrome-associated gene (MSAG). The predicted protein encoded by MSAG contains 110 amino acids and has a theoretical molecular weight of 11667.04 and an isoelectric point of 4.91. Compared with the housekeeping gene of beta-actin, MSAG had low transcription activity. However, the mRNA level of MSAG in HepG2 cells, a human hepatoma cell line, was significantly increased by glucose and decreased by insulin concentrations higher than physiological levels. These results suggest that MSAG may be involved in the metabolism and/or its regulation of glucose, the functioning of insulin under non-physiological conditions, and further in the development of metabolic syndrome.
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PMID:Identification of a novel gene, MSAG, regulated by high levels of glucose and insulin. 1923 44

Metabolic syndrome is a cluster of interconnected cardiovascular risk factors. This research determined the prevalence of metabolic syndrome by body mass index, sociodemography, and lifestyle habits of women 30-50 years old in Babol Iran. A systematic random sampling was used to select 984 middle aged women from an urban area in Babol, Mazandaran, Iran. Screening was used to select eligible women who fulfilled selection criteria. The Adult Treatment Panel III (ATP III) criteria were used to classify participants as having metabolic syndrome. The overall prevalence of metabolic syndrome was 31.0%. Abdominal obesity was observed in about 76.6% (n = 273) of subjects. The prevalences of hypertension, high fasting blood glucose, high triglycerides and low HDL-cholesterol were 12.1, 12.1, 41.5 and 48.6%, respectively. Older age (OR = 2.07; CI = 1.56-2.75), higher waist circumference (OR = 6.46; 95% CI = 3.48-11.96), higher systolic (OR = 3.84; 95% CI = 2.37-6.22) and diastolic blood pressure (OR = 1.89; 95% CI =1.17-3.05), low education level (OR = 2.780; CI = 1.80-4.31), housekeeping (OR = 3.92; CI = 1.24-12.44) and farming occupation (OR = 20.54; 95% CI = 3.54-119.06) were associated with increased risk for metabolic syndrome. The odds ratio (OR) showed no significant associations between metabolic syndrome and smoking or exposure to smoking. This study showed high prevalence of metabolic syndrome in Iranian middle aged women. A larger area and population study is needed to enable broader recommendations for the prevention of metabolic syndrome.
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PMID:Prevalence of metabolic syndrome among middle aged women in Babol, Iran. 1984 50

Autophagy is a housekeeping process that helps to maintain cellular energy homeostasis and remove damaged organelles. In the heart, autophagy is an adaptive process that is activated in response to stress including acute and chronic ischemia. Given the evidence that autophagy is suppressed in energy-rich conditions, the objective of this review is to examine autophagy and cardioprotection in the setting of the metabolic syndrome. Clinical approaches that involve the induction of cardiac autophagy pharmacologically to enhance the heart's tolerance to ischemia are also discussed.
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PMID:Autophagy, myocardial protection, and the metabolic syndrome. 2247 9

Ribonucleic acids (RNAs) are very complex and their all functions have yet to be fully clarified. Noncoding genes (noncoding RNA, sequences, and pseudogenes) comprise 67% of all genes and they are represented by housekeeping noncoding RNAs (transfer RNA (tRNA), ribosomal RNA (rRNA), small nuclear RNA (snRNA), and small nucleolar RNA (snoRNA)) that are engaged in basic cellular processes and by regulatory noncoding RNA (short and long noncoding RNA (ncRNA)) that are important for gene expression/transcript stability. In this review, we summarize data concerning the significance of long noncoding RNAs (lncRNAs) in metabolic syndrome related disorders, focusing on adipose tissue and pancreatic islands.
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PMID:Long Noncoding RNAs in Metabolic Syndrome Related Disorders. 2788 4

With the lack of success and increasing urgency for therapies capable of impacting Alzheimer's disease (AD) and its progression, there are increasing efforts to expand testing of new mechanistic hypotheses to attack the disease from different angles. Three such hypotheses are the "Mitochondrial Cascade (MC)" hypothesis, the "Endo-Lysosomal Dysfunction (ELD)" hypothesis and the "Type 3 Diabetes (T3D)" hypothesis. These hypotheses provide a rationale for new pharmacological approaches to address the mitochondrial, endo-lysosomal and metabolic dysfunction associated with AD. It is increasingly evident that there is critical interplay between the metabolic dysfunction associated with obesity/metabolic syndrome/type 2 diabetes mellitus (T2DM) and patient susceptibility to AD development. A candidate for a common mechanism linking these metabolically-driven disease states is chronically-activated mechanistic target of rapamycin (mTOR) signaling. Unrestrained chronic mTOR activation may be responsible for sustaining metabolic, lysosomal and mitochondrial dysfunction in AD, driving both the breakdown of the blood-brain barrier via endothelial cell dysfunction and hyperphosphorylation of tau and formation of amyloid plaques in the brain. It is hypothesized that sodium glucose cotransporter 2 (SGLT2) inhibition, mediated by sustained glucose loss, restores mTOR cycling through nutrient-driven, nightly periods of transient mTOR inhibition (and restoration of catabolic cellular housekeeping processes) interspersed by daily periods of transient mTOR activation (and anabolism) accompanying eating. In this way, a flexible mTOR dynamic is restored, thereby preventing or even reducing the progress of AD pathology. The first study to investigate the effect of SGLT2 inhibition in patients with AD is ongoing and focuses on the impact on energy metabolism in the brain following treatment with the SGLT2 inhibitor dapagliflozin.
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PMID:A role for sodium glucose cotransporter 2 inhibitors (SGLT2is) in the treatment of Alzheimer's disease? 3285 52