Chronic Fructose Ingestion as a Major Health Concern: Is a Sedentary Lifestyle Making It Worse? A Review.

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Term Occurence Count Dictionary
Insulin 3 endocrinologydiseasesdrugs
glucose intolerance 2 endocrinologydiseases
hyperuricemia 3 endocrinologydiseases
obesity 9 endocrinologydiseases
hyperglycemia 1 endocrinologydiseases
hyperinsulinemia 1 endocrinologydiseases
hyperlipidemia 7 endocrinologydiseases
hypertriglyceridemia 2 endocrinologydiseases
metabolic syndrome 15 endocrinologydiseases

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Select Drug Character Offset Drug Term Instance
Insulin 19893 glycerol-3-phosphate; and (3) fructose enhancing DNL when subsequent meals were ingested [[19],[20]].5. Fructose and Insulin ResistanceType 2 diabetes is a progressive disorder that begins with the development of insulin resistance
Insulin 22120 suppression no longer occurs, causing a subsequent increase in glucose output from the liver [[29]]. Insulin resistance in fat cells reduces the normal effects of insulin on lipids and results in reduced uptake
Insulin 25210 signaling cascade which involves Akt/PKB (protein kinase B) stimulation of glucose uptake into the cell. Insulin sensitivity is thus maintained as a result of enhanced glycogen synthesis, suppression of hepatic gluconeogenesis,
Select Disease Character Offset Disease Term Instance
glucose intolerance 486 contributes to metabolic abnormalities such as insulin resistance, dyslipidemia, hypertension, and glucose intolerance , all of which are risk factors associated with metabolic syndrome. The growing prevelance of metabolic
glucose intolerance 27324 humans, there is limited research confirming the negative effects of fructose on insulin sensitivity and glucose intolerance in adults and adolescents. Sunehag et al. [[41]] discovered no change in insulin sensitivity or secretion
hyperglycemia 22885 insulin, resulting in hyperinsulinemia. Since the β-cells cannot compensate for the resistant state, hyperglycemia occurs. Hyperglycemia further damages the β-cells, resulting in glycotoxicity, leading to a progressive
hyperinsulinemia 22805 insulin resistance, the pancreatic β-cells increase in mass and secrete more insulin, resulting in hyperinsulinemia . Since the β-cells cannot compensate for the resistant state, hyperglycemia occurs. Hyperglycemia further
hyperlipidemia 10412 there is an abundance of research indicating that acute and/or chronic ingestion of fructose causes hyperlipidemia in rats [[14],[16],[17]] and in humans [[18],[19],[20],[21]]. Faeh et al. [[21]] discovered that after
hyperlipidemia 11313 fructose-fed group were significantly higher than the starch group, indicating that fructose induced hyperlipidemia can occur in as little as 24 h after the first fructose load [[22]]. In a slightly longer intervention,
hyperlipidemia 15904 determinant in this process [[25]].4. Fructose and Postprandial LipemiaAlthough research regarding fasting hyperlipidemia and fructose consumption has been well established, high postprandial triglyceride levels have been
hyperlipidemia 33084 cardiovascular disease.Previous studies have shown that increased consumption of fructose results in hyperlipidemia accompanied by insulin resistance and elevated plasma TGs, all leading to increased inflammation [[21],[52],[53]].
hyperlipidemia 37574 [[60]]. Therefore, preventing metabolic risk factors such as coronary artery disease, type 2 diabetes and hyperlipidemia can be accomplished by incorporating moderate activity into a person’s daily routine in order to avoid
hyperlipidemia 51883 of fructose leads to various risk factors associated with metabolic syndrome such as hypertension, hyperlipidemia , insulin resistance, inflammation and hyperuricemia, there is still numerous contradictory evidence
hyperlipidemia 53190 fructose-induced metabolic alterations related to metabolic syndrome. These risk factors, such as postprandial hyperlipidemia , insulin resistance, and hyperuricemia, seem to be exacerbated with fructose ingestion in a dose-dependent
hypertriglyceridemia 17800 clearance with chronic fructose ingestion might also contribute to the fructose-induced postprandial hypertriglyceridemia that is often evident in fructose-fed individuals [[19]]. Other studies have shown similar results in
hypertriglyceridemia 19228 lipoprotein lipase-mediated clearance may be a contributing factor to fructose-induced postprandial hypertriglyceridemia [[19],[20]]. Although more research needs to be conducted in the postprandial state, when fructose is
hyperuricemia 3297 metabolic changes that may contribute to risk factors associated with metabolic syndrome as well as hyperuricemia , inflammation, and alterations in various metabolic hormones [[4]]. Today, the average American consumes
hyperuricemia 51936 with metabolic syndrome such as hypertension, hyperlipidemia, insulin resistance, inflammation and hyperuricemia , there is still numerous contradictory evidence which states that as long as fructose is consumed in
hyperuricemia 53230 metabolic syndrome. These risk factors, such as postprandial hyperlipidemia, insulin resistance, and hyperuricemia , seem to be exacerbated with fructose ingestion in a dose-dependent manner; hence continued research
metabolic syndrome 553 dyslipidemia, hypertension, and glucose intolerance, all of which are risk factors associated with metabolic syndrome . The growing prevelance of metabolic syndrome seems to be an end result of our current lifestyle which
metabolic syndrome 599 intolerance, all of which are risk factors associated with metabolic syndrome. The growing prevelance of metabolic syndrome seems to be an end result of our current lifestyle which promotes high caloric, high-fat foods and minimal
metabolic syndrome 1063 disturbances associated with diet and exercise habits is a crucial step towards reducing the risk factors for metabolic syndrome . Although considerable research has been conducted linking chronic fructose ingestion to the increased
metabolic syndrome 1211 research has been conducted linking chronic fructose ingestion to the increased prevalence of obesity and metabolic syndrome risk factors, these studies have mainly been performed on animals, and/or in a post-absorptive state.
metabolic syndrome 2137 33% obese [[1]]. Moderate obesity can contribute to chronic metabolic abnormalities characteristic of metabolic syndrome which include insulin resistance, dyslipidemia and hypertension [[2]]. Increased consumption of added
metabolic syndrome 3114 been an increased interest in the potential role of these added sugars as a contributing factor to metabolic syndrome . When consumed in elevated concentrations, fructose can promote metabolic changes that may contribute
metabolic syndrome 3267 concentrations, fructose can promote metabolic changes that may contribute to risk factors associated with metabolic syndrome as well as hyperuricemia, inflammation, and alterations in various metabolic hormones [[4]]. Today,
metabolic syndrome 3774 the form of sucrose or HFCS, may cause substantial alterations in the risk factors associated with metabolic syndrome . Furthermore, partaking in an inactive lifestyle will also be addressed as increased physical inactivity
metabolic syndrome 39312 of 60 years who reported high levels of sedentary behavior, had a greater prevalence of developing metabolic syndrome [[67]]. This data provides evidence that reducing prolonged overall sitting time may reduce metabolic
metabolic syndrome 48055 bout of exercise. However, IL-6 may actually help to prevent or reduce risk factors associated with metabolic syndrome and type 2 diabetes in the long-term [[75]]. During exercise, the magnitude of the increase in IL-6
metabolic syndrome 51429 were ameliorated [[81]]. Hence, increased physical activity may improve features of fructose-induced metabolic syndrome . More studies on humans still need to be conducted to determine the interaction between fructose consumption
metabolic syndrome 51842 ConclusionsAlthough it seems apparent that increased intake of fructose leads to various risk factors associated with metabolic syndrome such as hypertension, hyperlipidemia, insulin resistance, inflammation and hyperuricemia, there is still
metabolic syndrome 52697 Although fructose consumption cannot be completely to blame for the increased rates of obesity and metabolic syndrome , fructose is often associated with additional detrimental behaviors such as a hypercaloric diet, or
metabolic syndrome 52927 in saturated fats, as well as low physical activity [[6]]. These behaviors lead to risk factors of metabolic syndrome , and as such could be prevented and/or reduced.The above review of literature summarizes the proposed
metabolic syndrome 53129 summarizes the proposed mechanisms associated with the fructose-induced metabolic alterations related to metabolic syndrome . These risk factors, such as postprandial hyperlipidemia, insulin resistance, and hyperuricemia, seem
obesity 1199 considerable research has been conducted linking chronic fructose ingestion to the increased prevalence of obesity and metabolic syndrome risk factors, these studies have mainly been performed on animals, and/or in
obesity 1888 investigate whether increased physical activity can alter such effects.1. IntroductionThe prevalence of obesity and obesity-related diseases in the United State and worldwide is increasing rapidly, with 67% of the
obesity 1900 whether increased physical activity can alter such effects.1. IntroductionThe prevalence of obesity and obesity -related diseases in the United State and worldwide is increasing rapidly, with 67% of the population
obesity 2061 increasing rapidly, with 67% of the population considered overweight and 33% obese [[1]]. Moderate obesity can contribute to chronic metabolic abnormalities characteristic of metabolic syndrome which include
obesity 36065 accumulation within the liver may induce a sub-acute inflammatory response that is similar to that seen in obesity -related inflammation within adipocytes. TNF-α, IL-6 and IL-1β, all pro-inflammatory markers, are overproduced
obesity 39719 [[66]]. Data from the Medical Expenditure Panel Survey indicated that both physical inactivity and obesity are strongly and independently correlated with diabetes and cardiovascular disease [[68]]. According
obesity 40042 (BMI), indicating that it is better to be active than inactive. Hence, both physical inactivity and obesity seem to be independently associated with diabetes and diabetes-related risk factors [[68]]. Moreover,
obesity 47871 [[77]]. Although low-grade inflammation, characteristic of elevated IL-6 levels, has been associated with obesity and insulin resistance, it is markedly produced and released after an acute bout of exercise. However,
obesity 52685 these risks. Although fructose consumption cannot be completely to blame for the increased rates of obesity and metabolic syndrome, fructose is often associated with additional detrimental behaviors such as a

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