Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans.
By K. Stanhope, J. Schwarz, N. Keim, S. Griffen, A. Bremer, J. Graham, B. Hatcher, C. L. Cox, A. Dyachenko, Wei Zhang and 13 more. Journal of Clinical Investigation, 2009
1,700 citations recorded by the source corpus.
Subfields: Endocrinology, Diabetes and Metabolism, Epidemiology, Physiology
View Paper: https://www.semanticscholar.org/paper/00835f2413b5cc325bcae974e2f3f7222ff17506
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Endocrinology, Diabetes and Metabolism
- F. B. Hu
- Vasanti S. Malik
- André Tchernof
- W. Willett
- I. Graham
- J. Despres
- Gerald I. Shulman
- Barry M. Popkin
In Epidemiology
- Herbert Tilg
- André Tchernof
- A. Moschen
- V. Samuel
- Gerald I. Shulman
- Barry M. Popkin
- Lina Badimon
- J. Despres
In Physiology
- F. B. Hu
- V. Samuel
- Frank B Hu
- W. Willett
- Vasanti S. Malik
- I. Graham
- Gerald I. Shulman
- Rhian M. Touyz
Citations in the corpus
- ESC/EAS Guidelines for the management of dyslipidaemias: the Task Force for the management of dyslipidaemias of the European Society of Cardiology (ESC) and the European Atherosclerosis Society (EAS). (2011, background): “Sucrose, a disaccharide containing glucose and fructose, represents an important source of fructose in the diet.(76)”
- Evolution of inflammation in nonalcoholic fatty liver disease: The multiple parallel hits hypothesis (2010, background): “When obese subjects consumed glucoseor fructose-sweetened beverages for 10 weeks, fasting plasma glucose and insulin levels increased and insulin sensitivity decreased in subjects consuming fructose but not in those consuming glucose.(31) Daily fructose consumption is associated with increased hepat”
- The pathogenesis of insulin resistance: integrating signaling pathways and substrate flux. (2016, background): “Human subjects who consumed fructose-containing beverages, in comparison with those consuming isocaloric glucose-containing beverages, developed hyperlipidemia and insulin resistance despite gaining a similar amount of weight (113).”
- 2016 ESC/EAS Guidelines for the Management of Dyslipidaemias. (2016, background): “the general population and should be drastically limited in those individuals with elevated TG values.(158,159)”
- Sugar-Sweetened Beverages and Risk of Metabolic Syndrome and Type 2 Diabetes (2010, background): “Additional metabolic effects of these beverages may also lead to hypertension, promote accumulation of visceral adipose tissue and of ectopic fat due to elevated hepatic de novo lipogenesis(10) leading to the development of the high triglycerides, low HDL-cholesterol and small dense LDL, although th”
- Nutrition Therapy Recommendations for the Management of Adults With Diabetes (2013, neutral): “Evidence suggests that consuming high levels of fructose-containing beverages may have particularly adverse effects on selective deposition of ectopic and visceral fat, lipid metabolism, blood pressure, insulin sensitivity, and de novo lipogenesis, compared with glucose-sweetened beverages (142).”
- Sugar-sweetened beverages and risk of obesity and type 2 diabetes: Epidemiologic evidence (2010, background): “In a recent study comparing the effects of consuming glucose or fructose sweetened beverages providing 25% of energy requirements, after 10-weeks, both groups showed similar weight gain, but only the fructose group showed a significant increase in visceral adiposity [22].”
- Sugar, Uric Acid, and the Etiology of Diabetes and Obesity (2013, background): “Although some features of metabolic syndrome were induced with glucose, the fructose-fed subjects showed worse postprandial hypertriglyceridemia, increased hepatic de novo synthesis of fatty acids, a decrease in insulin sensitivity (noted by elevations in fasting glucose and insulin levels), increas”