2009
DOI: 10.1210/jc.2008-2192
|View full text |Cite
|
Sign up to set email alerts
|

Endocrine and Metabolic Effects of Consuming Fructose- and Glucose-Sweetened Beverages with Meals in Obese Men and Women: Influence of Insulin Resistance on Plasma Triglyceride Responses

Abstract: In obese subjects, consumption of fructose-sweetened beverages with meals was associated with less insulin secretion, blunted diurnal leptin profiles, and increased postprandial TG concentrations compared with glucose consumption. Increases of TGs were augmented in obese subjects with insulin resistance, suggesting that fructose consumption may exacerbate an already adverse metabolic profile present in many obese subjects.

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
3
1
1

Citation Types

10
119
2
3

Year Published

2013
2013
2022
2022

Publication Types

Select...
8
1

Relationship

0
9

Authors

Journals

citations
Cited by 257 publications
(134 citation statements)
references
References 38 publications
10
119
2
3
Order By: Relevance
“…Since that publication, other epidemiologic studies have shown that chronic consumption of sugar-sweetened beverages are associated with greater rates of obesity, insulin resistance, type 2 diabetes, and heart disease (Bray et al 2004;Bremer et al 2010;Fung et al 2009;Montonen et al 2007;Palmer et al 2008;Schulze et al 2004;Yoshida et al 2007). Experimental studies have compared the metabolic health effects of different sugar-sweetened beverages O including pure glucose, pure fructose, HFCS, and sucrose O at various doses of sugar intake and consumed for various lengths of time (1 day to 10 weeks) (Aeberli et al 2011(Aeberli et al , 2013Cox et al 2011Cox et al , 2012Le et al 2006;Stanhope et al 2008Stanhope et al , 2009Stanhope et al , 2011aStanhope et al , 2011bSwarbrick et al 2008;Teff et al 2009). These studies have demonstrated that the 2 common sweeteners, HFCS and sucrose, have similar metabolic effects, and that fructosesweetened beverages are more detrimental to metabolic health than glucose-sweetened beverages, because fructose-sweetened beverages have been shown to increase proinflammatory and prothrombotic mediators, postprandial triacylglycerol (TAG) concentrations, uric acid concentrations, and intrahepatocellular lipids, and to reduce hepatic insulin sensitivity to a greater extent than glucose-sweetened beverages (Aeberli et al 2011(Aeberli et al , 2013Cox et al 2011Cox et al , 2012Le et al 2006;Stanhope et al 2008Stanhope et al , 2009Stanhope et al , 2011aStanhope et al , 2011bSwarbrick et al 2008;Teff et al 2009).…”
Section: Introductionmentioning
confidence: 99%
“…Since that publication, other epidemiologic studies have shown that chronic consumption of sugar-sweetened beverages are associated with greater rates of obesity, insulin resistance, type 2 diabetes, and heart disease (Bray et al 2004;Bremer et al 2010;Fung et al 2009;Montonen et al 2007;Palmer et al 2008;Schulze et al 2004;Yoshida et al 2007). Experimental studies have compared the metabolic health effects of different sugar-sweetened beverages O including pure glucose, pure fructose, HFCS, and sucrose O at various doses of sugar intake and consumed for various lengths of time (1 day to 10 weeks) (Aeberli et al 2011(Aeberli et al , 2013Cox et al 2011Cox et al , 2012Le et al 2006;Stanhope et al 2008Stanhope et al , 2009Stanhope et al , 2011aStanhope et al , 2011bSwarbrick et al 2008;Teff et al 2009). These studies have demonstrated that the 2 common sweeteners, HFCS and sucrose, have similar metabolic effects, and that fructosesweetened beverages are more detrimental to metabolic health than glucose-sweetened beverages, because fructose-sweetened beverages have been shown to increase proinflammatory and prothrombotic mediators, postprandial triacylglycerol (TAG) concentrations, uric acid concentrations, and intrahepatocellular lipids, and to reduce hepatic insulin sensitivity to a greater extent than glucose-sweetened beverages (Aeberli et al 2011(Aeberli et al , 2013Cox et al 2011Cox et al , 2012Le et al 2006;Stanhope et al 2008Stanhope et al , 2009Stanhope et al , 2011aStanhope et al , 2011bSwarbrick et al 2008;Teff et al 2009).…”
Section: Introductionmentioning
confidence: 99%
“…In healthy non-obese women, the VAT area assessed through CT has been estimated to increase with age at a rate of 2.36 cm 2 per year [16]. Recent studies have demonstrated that fructose consumption increases TG and glucose levels, leading to insulin resistance and exacerbating the metabolic profile presentation [17]. Moreover, fructose consumption among overweight individuals is reported to increase de novo lipogenesis, dyslipidemia, and visceral adiposity, and to decrease insulin sensitivity [18].…”
Section: Discussionmentioning
confidence: 99%
“…For these studies, the cell culture media monosaccharide content of 0.72 mmol/L (glucose alone or glucose plus fructose) was found to maximize hepatocellular lipogenesis. This molar amount was determined following a series of experiments, employing a step-wise increase in sugar content and based on previous human studies showing serum total monosaccharide concentrations of approximately 0.50 mmol/L following a fructose-rich meal [24] . Higher amounts of monosaccharide (> 0.72 mmol/L) in the Huh7 incubating media did not yield statistically significant increases either in cellular TG or in cellular C content, while further increases (> 400 mmol/L) in media osmolality resulted in decreased cell viability.…”
Section: Discussionmentioning
confidence: 99%
“…As stated previously, a recent meta-analysis concluded the potential association between fructose and NAFLD was confounded by the concurrent consumption of hypercaloric diets [12] . The influence of fructose on lipogenesis, as a consequence of excess energy intake, may be mediated by this monosaccharide's direct attenuation of post-prandial ghrelin suppression [24] . On the other hand, another study examining the effects of dietary sucrose vs HFCS on endogenous hormone levels, failed to demonstrate any significant differences in serum insulin, leptin and ghrelin levels [25] .…”
Section: Discussionmentioning
confidence: 99%