High Dietary Fructose: Direct or Indirect Dangerous Factors Disturbing Tissue and Organ Functions

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Term Occurence Count Dictionary
Insulin 8 endocrinologydiseasesdrugs
hyperglycemia 1 endocrinologydiseases
hyperinsulinemia 1 endocrinologydiseases
hyperlipidemia 2 endocrinologydiseases
hyperuricemia 6 endocrinologydiseases
metabolic syndrome 6 endocrinologydiseases
glucose intolerance 1 endocrinologydiseases
hypertriglyceridemia 2 endocrinologydiseases
obesity 6 endocrinologydiseases

Graph of close proximity drug and disease terms (within 200 characters).

Note: If this graph is empty, then there are no terms that meet the proximity constraint.

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Select Drug Character Offset Drug Term Instance
Insulin 47382 production Inflammatory cytokine flux FFA uptake Adiponectin secretion Lipid accumulation Autophagy Insulin sensitivity Leptin sensitivity Glucose uptake Oxygen availabilityPKCθ/IKK-β/c-JNK [[39],[40],[41]]
Insulin 47725 [[135]]BrainAppetite increase Psychological stressFFA UA MGROS production Inflammation cytokine flux Food intake Insulin sensitivity Leptin sensitivityTNF-α/AMPK/malonyl-CoA [[76],[77]] NLRP3/NF-κB [[95]] TLR4/NF-κB, FKN/CX3CR1
Insulin 48026 formation Vascular stiffnessFFA UAROS production FFA uptake Vascular tone RAGE production Blood pressure Insulin sensitivity Glucose consumption Vascular vasodilationHK/PFK [[22]] FATPs/CD36 [[61]] CD36/TLR4/6/IRAK4/1/NLRP3
Insulin 48360 permeabilityUAEndotoxin translocation Bacterial composition disturbance Dysregulation of tight junction protein Insulin sensitivitySR-BI/ERK/ApoB [[80]] KHK/Occludin and ZO-1 [[173],[174]]KidneyCKD Endothelial dysfunctionUA
Insulin 48600 Inflammatory cytokine flux Dysregulation of renal organic ion transporters NO production Urine sodium retention Insulin sensitivity UA clearanceHK/PFK [[22]] XO/eNOS [[110],[111]] NLRP3/NF-κB [[92],[93],[94],[96]] PGE2/Organic
Insulin 49049 production DNL Inflammatory cytokine flux Lipid accumulation Mitochondrial dysfunction VLDL-secretion Insulin sensitivity Glucose consumption Glucose uptake Oxygen availabilityIRS/PI3K/Akt, ChREBP/SCD-1 [[11]]
Insulin 49679 β-cell mass Irregular insulin secretionGlucose FFA UAInflammatory cytokines flux ER stress Apoptosis Insulin sensitivity Leptin sensitivityTR [[14]] Akt/FoxO1 [[15]] SREBP-1c/IRS-2/Akt [[44]]Cideb [[48]] FFAR1
Insulin 49973 dysfunctionLactate FFA Ceramide UAROS production FFA uptake Autophagy Inflammatory cytokine flux Lipid accumulation Insulin sensitivity Glucose uptake Oxygen availabilityPI3K/Akt [[21]] HK/PFK [[22]] GLUT4 [[23],[24]] FATPs/CD36
Select Disease Character Offset Disease Term Instance
glucose intolerance 9673 associated with insulin resistance, inflammation and abnormal lipid metabolism, possibly leading to glucose intolerance and insulin resistance [[13]].3.2. LactateHigh fructose increases postprandial lactate level, leading
hyperglycemia 13597 activating insulin receptor substrate (IRS)-1/2/PI3K/Akt pathway [[11]]; this pathway impairment causes hyperglycemia and compensatory hyperinsulinemia, cooperatively preceding systemic insulin resistance. Fructose feeding
hyperinsulinemia 13628 substrate (IRS)-1/2/PI3K/Akt pathway [[11]]; this pathway impairment causes hyperglycemia and compensatory hyperinsulinemia , cooperatively preceding systemic insulin resistance. Fructose feeding may upregulate hepatic carbohydrate
hyperlipidemia 12421 and/or local insulin resistance.3.3. Free Fatty Acids (FFAs)High fructose consumption gives rise to hyperlipidemia [[29]]. Significant increase in hepatic DNL is one of the major adverse causes for metabolic burden
hyperlipidemia 12632 burden under high fructose consumption. Therefore, increased plasma FFAs, TG and VLDL-TG levels induce hyperlipidemia , as well as TG accumulation in extrahepatic tissues and organs. Fructose-induced lipotoxicity leads
hypertriglyceridemia 18018 liver. PKC activation is also detected in adipose tissue, which may be associated with fructose-induced hypertriglyceridemia [[52]].Fructose supplementation increases de novo ceramide biosynthesis and elevates ceramide concentrations
hypertriglyceridemia 23527 components of VLDL in circulation, is observed under high fructose diet [[84]]. Elevated apoC-III induces hypertriglyceridemia [[85]] and insulin resistance [[86]], acting as another emerging pro-atherosclerosis factor. Moreover,
hyperuricemia 2480 hypertension, cardiovascular disease (CVD), type 2 diabetes (T2DM), non-alcoholic fatty liver (NAFLD), hyperuricemia , gout and chronic kidney disease (CKD) [[3]].Fructose is a monosaccharide found in fruits, vegetables
hyperuricemia 24531 catabolism in liver induces rapidly ATP depletion to overproduce UA in systemic circulation, developing hyperuricemia in humans and experimental animals [[89]]. Epidemiological studies reveal that hyperuricemia has close
hyperuricemia 24624 developing hyperuricemia in humans and experimental animals [[89]]. Epidemiological studies reveal that hyperuricemia has close relationship with insulin resistance, inducing gout, hypertension, atherosclerosis and chronic
hyperuricemia 25871 kidney and hypothalamus [[101],[102],[103],[104]]. Furthermore, ROS generation under fructose-induced hyperuricemia is the crucial factor for podocyte injury by activating p38 MAPK/thioredoxin-interacting protein (TXNIP)/NLRP3
hyperuricemia 27131 inflammation by high UA-induced ROS generation.UA-induced endothelial dysfunction is another adverse burden in hyperuricemia [[108]], which may promote insulin resistance and cardiovascular disease under high fructose consumption.
hyperuricemia 28755 transporter 1 (OAT1), OAT3, and urate transporter (UAT), which cause abnormal renal UA excretion involved in hyperuricemia and renal dysfunction [[114]]. Meanwhile, upregulation of renal prostaglandin E2 (PGE2), a primary mediator
metabolic syndrome 475 (collection): 4/2017AbstractHigh dietary fructose is a major contributor to insulin resistance and metabolic syndrome , disturbing tissue and organ functions. Fructose is mainly absorbed into systemic circulation by glucose
metabolic syndrome 1369 endothelial dysfunction, autophagy and increased intestinal permeability, and then further aggravate the metabolic syndrome with tissue and organ dysfunctions. Therefore, this review addresses fructose-induced metabolic syndrome,
metabolic syndrome 1474 metabolic syndrome with tissue and organ dysfunctions. Therefore, this review addresses fructose-induced metabolic syndrome , and the disturbance effects of direct and/or indirect dangerous factors on the functions of liver,
metabolic syndrome 1895 under excess dietary fructose consumption. 1. IntroductionThe World Health Organization (WHO) defines metabolic syndrome (MetS) as a cluster of symptoms with impaired glucose tolerance or insulin resistance, together with
metabolic syndrome 44341 added to commercial food additives. Overconsumption of fructose is a risk factor for the epidemic of metabolic syndrome (MetS), with dysfunctions in multiple tissues and organs including liver, adipose, pancreatic islet,
metabolic syndrome 46609 endothelial dysfunction, autophagy and increased intestinal permeability, and then further aggravate metabolic syndrome with tissue and organ dysfunctions. DHAP, dihydroxyacetone phosphate; TG: triglyceride; FFA: free fatty
obesity 2177 pressure, raised plasma triglyceride (TG) and/or low high-density lipoprotein (HDL) cholesterol, central obesity and microalbuminuria [[1]]. Central obesity and insulin resistance are acknowledged as the important
obesity 2221 low high-density lipoprotein (HDL) cholesterol, central obesity and microalbuminuria [[1]]. Central obesity and insulin resistance are acknowledged as the important causative factors in the pathogenesis of MetS
obesity 22112 triggers AMPK/malonyl-CoA signaling in hypothalamus, subsequently increasing food intake and the risk of obesity [[77]]. Furthermore, fructose-induced hypothalamic AMPK activation increases hepatic gluconeogenesis
obesity 35433 proliferator-activated receptor (PPAR)-δ, one of the most promising pharmacological targets implicated in obesity -associated insulin resistance, is highly expressed in skeletal muscle. Fructose-induced disturbance
obesity 38846 cause adiponectin secretion reduction [[151]].Relevant work reports the crucial role of adiponectin in obesity and liver disease. Serum adiponectin concentration is decreased in rodents with increased influx of
obesity 39201 mice, fructose consumption does not change insulin sensitivity, adiponectin sensitivity and visceral obesity , indicating that the burden of MetS is closely associated with fructolysis [[157]]. Adiponectin receptor

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