Abstract
PURPOSE OF REVIEW: Based on interim results from an ongoing study, we have reported that consumption of a high-fructose diet, but not a high-glucose diet, promotes the development of three of the pathological characteristics associated with metabolic syndrome: visceral adiposity, dyslipidemia, and insulin resistance. From these results and a review of the current literature, we present two potential sequences of events by which fructose consumption may contribute to metabolic syndrome. RECENT FINDINGS: The earliest metabolic perturbation resulting from fructose consumption is postprandial hypertriglyceridemia, which may increase visceral adipose deposition. Visceral adiposity contributes to hepatic triglyceride accumulation, novel protein kinase C activation, and hepatic insulin resistance by increasing the portal delivery of free fatty acids to the liver. With insulin resistance, VLDL production is upregulated and this, along with systemic free fatty acids, increase lipid delivery to muscle. It is also possible that fructose initiates hepatic insulin resistance independently of visceral adiposity and free fatty acid delivery. By providing substrate for hepatic lipogenesis, fructose may result in a direct lipid overload that leads to triglyceride accumulation, novel protein kinase C activation, and hepatic insulin resistance. SUMMARY: Our investigation and future studies of the effects of fructose consumption may help to clarify the sequence of events leading to development of metabolic syndrome.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 16-24 |
| Number of pages | 9 |
| Journal | Current Opinion in Lipidology |
| Volume | 19 |
| Issue number | 1 |
| DOIs | |
| State | Published - Feb 2008 |
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Keywords
- Dyslipidemia
- Free fatty acids
- Fructose consumption
- Hepatic steatosis
- Insulin resistance
- Metabolic syndrome
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)
Cite this
Fructose consumption : Potential mechanisms for its effects to increase visceral adiposity and induce dyslipidemia and insulin resistance. / Stanhope, Kimber; Havel, Peter J.
In: Current Opinion in Lipidology, Vol. 19, No. 1, 02.2008, p. 16-24.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Fructose consumption
T2 - Potential mechanisms for its effects to increase visceral adiposity and induce dyslipidemia and insulin resistance
AU - Stanhope, Kimber
AU - Havel, Peter J
PY - 2008/2
Y1 - 2008/2
N2 - PURPOSE OF REVIEW: Based on interim results from an ongoing study, we have reported that consumption of a high-fructose diet, but not a high-glucose diet, promotes the development of three of the pathological characteristics associated with metabolic syndrome: visceral adiposity, dyslipidemia, and insulin resistance. From these results and a review of the current literature, we present two potential sequences of events by which fructose consumption may contribute to metabolic syndrome. RECENT FINDINGS: The earliest metabolic perturbation resulting from fructose consumption is postprandial hypertriglyceridemia, which may increase visceral adipose deposition. Visceral adiposity contributes to hepatic triglyceride accumulation, novel protein kinase C activation, and hepatic insulin resistance by increasing the portal delivery of free fatty acids to the liver. With insulin resistance, VLDL production is upregulated and this, along with systemic free fatty acids, increase lipid delivery to muscle. It is also possible that fructose initiates hepatic insulin resistance independently of visceral adiposity and free fatty acid delivery. By providing substrate for hepatic lipogenesis, fructose may result in a direct lipid overload that leads to triglyceride accumulation, novel protein kinase C activation, and hepatic insulin resistance. SUMMARY: Our investigation and future studies of the effects of fructose consumption may help to clarify the sequence of events leading to development of metabolic syndrome.
AB - PURPOSE OF REVIEW: Based on interim results from an ongoing study, we have reported that consumption of a high-fructose diet, but not a high-glucose diet, promotes the development of three of the pathological characteristics associated with metabolic syndrome: visceral adiposity, dyslipidemia, and insulin resistance. From these results and a review of the current literature, we present two potential sequences of events by which fructose consumption may contribute to metabolic syndrome. RECENT FINDINGS: The earliest metabolic perturbation resulting from fructose consumption is postprandial hypertriglyceridemia, which may increase visceral adipose deposition. Visceral adiposity contributes to hepatic triglyceride accumulation, novel protein kinase C activation, and hepatic insulin resistance by increasing the portal delivery of free fatty acids to the liver. With insulin resistance, VLDL production is upregulated and this, along with systemic free fatty acids, increase lipid delivery to muscle. It is also possible that fructose initiates hepatic insulin resistance independently of visceral adiposity and free fatty acid delivery. By providing substrate for hepatic lipogenesis, fructose may result in a direct lipid overload that leads to triglyceride accumulation, novel protein kinase C activation, and hepatic insulin resistance. SUMMARY: Our investigation and future studies of the effects of fructose consumption may help to clarify the sequence of events leading to development of metabolic syndrome.
KW - Dyslipidemia
KW - Free fatty acids
KW - Fructose consumption
KW - Hepatic steatosis
KW - Insulin resistance
KW - Metabolic syndrome
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UR - http://www.scopus.com/inward/citedby.url?scp=38149042079&partnerID=8YFLogxK
U2 - 10.1097/MOL.0b013e3282f2b24a
DO - 10.1097/MOL.0b013e3282f2b24a
M3 - Article
C2 - 18196982
AN - SCOPUS:38149042079
VL - 19
SP - 16
EP - 24
JO - Current Opinion in Lipidology
JF - Current Opinion in Lipidology
SN - 0957-9672
IS - 1
ER -