Fructose, Glucocorticoids and Adipose Tissue: Implications for the Metabolic Syndrome.

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cortisol 6 endocrinologydiseasesdrugs
diabetes mellitus 1 endocrinologydiseases
febuxostat 1 endocrinologydiseasesdrugs
hyperglycemia 2 endocrinologydiseases
hypertriglyceridemia 1 endocrinologydiseases
metabolic syndrome 3 endocrinologydiseases
obesity 26 endocrinologydiseases
Insulin 1 endocrinologydiseasesdrugs

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Insulin 11552 fructose was proposed to promote leptin resistance, worsening obesity and insulin resistance [[52]]. Insulin resistance may be a secondary cause of obesity upon consumption of a hyperenergetic and high fructose-containing
cortisol 5717 function as well as proliferation/differentiation [[26],[27]]. The intracellular active glucocorticoids ( cortisol and corticosterone are the major glucocorticoids in humans and rodents, respectively) are generated
cortisol 27811 hypertension [[115],[116]]. However, in abdominally obese patients without Cushing’s disease, circulating cortisol levels are not elevated [[115]]. However, individuals with essential abdominal obesity have an impaired
cortisol 28389 this indicates a higher hypothalamus-pituitary-adrenal (HPA) axis activity. Importantly, the local cortisol synthesis in adipose tissue was found to be increased and is recognized as an important etiologic factor
cortisol 28655 Intracellularly, 11β-HSD1 is responsible for the generation of physiologically active glucocorticoids ( cortisol , corticosterone) from their inert precursors (cortisone, 11-dehydrocorticosterone), thus regulating
cortisol 31512 alterations of the redox state of pyridine nucleotides are well mirrored by cortisone reduction and cortisol oxidation capacity [[29],[135]]. Over-nutrition with a high sugar load stimulates the local activation
cortisol 32006 consequently resulted in a shift from 11β-HSD1 oxoreductase to dehydrogenase activity, thereby lowering the cortisol /cortisone ratio. As reported earlier, at 1 g/L of glucose, 11β-HSD1 oxoreductase activity decreased
febuxostat 20924 diseases including stroke [[90],[91]]. Lowering the uric acid level using the xanthine oxidase inhibitor febuxostat prevented the fructose-induced development of MetS [[92]]. One suggested mechanism includes the direct
Select Disease Character Offset Disease Term Instance
diabetes mellitus 3006 Epidemiologic studies pointed out that overweight and obesity are important risk factors of type II diabetes mellitus (T2DM) and cardiovascular disease (CVD) [[3],[4],[5],[6]]. The involvement of adiposity—predominantly
hyperglycemia 29500 increased non-esterified fatty acid release. Conversely, transgenic 11β-HSD1 KO mice showed reduced hyperglycemia and VAT accumulation and improved insulin sensitivity compared to wild-type mice under conditions of
hyperglycemia 40835 the ALIOS diet in the study by Larner et al. [[145]], but 11β-HSD1 KO mice were resistant against hyperglycemia induced by obesity or stress in the study by Kotelevtsev et al. [[126]], remains unclear. Analysis of
hypertriglyceridemia 37072 tissue [[140]]. Importantly, these rats developed some of the characteristic features of MetS, such as hypertriglyceridemia and hypertension. Other investigators showed that a shorter exposure of 24 h to a high fructose diet
metabolic syndrome 2284 glucocorticoid activation in adipose tissue, and their metabolic effects on the progression of the metabolic syndrome .1. IntroductionOur ancestors obtained their food from hunting and gathering, but the transition to modern
metabolic syndrome 3175 [[3],[4],[5],[6]]. The involvement of adiposity—predominantly splanchnic obesity—in the development of the metabolic syndrome (MetS) has been well established [[7]]. Metabolic and endocrine factors, like hormones and para/autocrine
metabolic syndrome 19206 evidence that oxidative stress is implicated in fructose-mediated adiposity, insulin resistance, and metabolic syndrome . In a study in rats, fructose induced the mRNA and protein expression of ER stress markers, including
obesity 2822 meat, and sodium, as well as an excessive consumption of sugar [[1]]. In line with this transition, obesity has emerged as a major global health problem in the last few decades [[2]]. Epidemiologic studies pointed
obesity 2960 health problem in the last few decades [[2]]. Epidemiologic studies pointed out that overweight and obesity are important risk factors of type II diabetes mellitus (T2DM) and cardiovascular disease (CVD) [[3],[4],[5],[6]].
obesity 3139 cardiovascular disease (CVD) [[3],[4],[5],[6]]. The involvement of adiposity—predominantly splanchnic obesity —in the development of the metabolic syndrome (MetS) has been well established [[7]]. Metabolic and
obesity 3814 response is also a key factor for modulating insulin sensitivity in adipose tissue and the development of obesity -associated diseases [[10]]. The chronic low-grade inflammation is a characteristic of obesity, whereby
obesity 3908 development of obesity-associated diseases [[10]]. The chronic low-grade inflammation is a characteristic of obesity , whereby adipose tissue releases many inflammatory mediators, including TNF-α, IL-1β, and IL-6, and
obesity 4370 [[12],[13]], and numerous human and animal studies demonstrated a link to the rising prevalence of obesity , T2DM, and MetS [[14],[15],[16],[17]]. Fructose, which is found in fruits, became a major component
obesity 7862 association of a high sugar intake with T2DM, an effect that was modified but not confounded by overweight or obesity and that was not dependent on a sedentary lifestyle [[37]]. Furthermore, an analysis of dietary history
obesity 8466 Especially the consumption of sugar sweetened beverages have been regarded as critical for development of obesity , hypertension, and T2DM [[14],[40],[41],[42],[43]]. Another recent observational clinical study revealed
obesity 10448 glucose are combined with different fat diets. A critical issue remains that fructose consumption and obesity are linked and that so far no clear association between fructose intake and cardiometabolic disease
obesity 10717 overeating and weight gain [[40],[46],[47],[48]].According to another concept, fructose could contribute to obesity by stimulating sterol receptor element binding protein 1c (SREBP-1c) independently of insulin, which
obesity 11513 insulin resistance [[15]]. Additionally, fructose was proposed to promote leptin resistance, worsening obesity and insulin resistance [[52]]. Insulin resistance may be a secondary cause of obesity upon consumption
obesity 11599 resistance, worsening obesity and insulin resistance [[52]]. Insulin resistance may be a secondary cause of obesity upon consumption of a hyperenergetic and high fructose-containing diet [[53],[54]], again pointing to
obesity 11807 to the importance of dissecting the direct impact of fructose and the consequences of overeating and obesity . Thus, further studies are needed to address the effects of fructose and sucrose intake under isocaloric
obesity 11987 sucrose intake under isocaloric dietary regimens and in defined subgroups, including patients with obesity , T2DM, and CVD.An obesogenic effect of large doses of fructose was also observed in animal studies.
obesity 20682 uric acid have been associated with a series of pathological conditions, including insulin resistance, obesity , T2DM, and chronic kidney disease [[57],[89]] and have been proposed as a risk factor for myocardial
obesity 27586 Differentiation/ProliferationA systemic glucocorticoid excess, as observed in Cushing’s disease, leads to obesity and all further symptoms of the MetS, with a pathological phenotype of dyslipidemia, insulin resistance,
obesity 27899 circulating cortisol levels are not elevated [[115]]. However, individuals with essential abdominal obesity have an impaired diurnal glucocorticoid rhythm with lower peak levels but higher levels during nadir
obesity 28507 in adipose tissue was found to be increased and is recognized as an important etiologic factor for obesity -related diseases [[21],[33],[122]]. Intracellularly, 11β-HSD1 is responsible for the generation of
obesity 28920 mineralocorticoid receptors [[28],[29],[32],[34]]. It is known that 11β-HSD1 is elevated in adipose tissue in obesity [[122],[123]], where it can contribute to metabolic complications. In contrast, 11β-HSD1 expression
obesity 29098 contrast, 11β-HSD1 expression remained at normal levels or was found to be reduced in the liver in obesity and T2DM [[123],[124],[125]]. Investigations in transgene mice showed that a moderate overexpression
obesity 39660 and 42 g/L high fructose corn syrup (55% fructose, 45% glucose) in the drinking water) recapitulated obesity , insulin resistance, dyslipidemia, and the spectrum of nonalcoholic fatty liver disease (NAFLD) [[145]].
obesity 40860 study by Larner et al. [[145]], but 11β-HSD1 KO mice were resistant against hyperglycemia induced by obesity or stress in the study by Kotelevtsev et al. [[126]], remains unclear. Analysis of the differences in
obesity 41737 to be the most hypertriglyceridemic sugar. However, it is important to investigate whether abdominal obesity exacerbates the hypertriglyceridemic effect of the high fructose diet and whether increased glucocorticoids
obesity 41996 effects of high fructose. Independently of the consumed fructose, elevated glucocorticoids and central obesity , especially visceral obesity, are associated with a higher risk for T2DM and MetS. Therefore, future
obesity 42025 Independently of the consumed fructose, elevated glucocorticoids and central obesity, especially visceral obesity , are associated with a higher risk for T2DM and MetS. Therefore, future investigations on the effects
obesity 42308 (solid food or beverage) and should include careful controls regarding the sex-, genetics-, stress-, and obesity -related differences in responsiveness. The importance of the G6PT-H6PDH-11β-HSD1 system in the ER-lumen

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