Dietary fructose reduces circulating insulin and leptin, attenuates postprandial suppression of ghrelin, and increases triglycerides in women

Karen L. Teff, Sharon S. Elliott, Matthias Tschöp, Timothy J. Kieffer, Daniel Rader, Mark Heiman, Raymond R. Townsend, Nancy L. Keim, David D'Alessio, Peter J Havel

Research output: Contribution to journalArticle

463 Citations (Scopus)

Abstract

Previous studies indicate that leptin secretion is regulated by insulin-mediated glucose metabolism. Because fructose, unlike glucose, does not stimulate insulin secretion, we hypothesized that meals high in fructose would result in lower leptin concentrations than meals containing the same amount of glucose. Blood samples were collected every 30-60 min for 24 h from 12 normal-weight women on 2 randomized days during which the subjects consumed three meals containing 55, 30, and 15% of total kilocalories as carbohydrate, fat, and protein, respectively, with 30% of kilocalories as either a fructose-sweetened [high fructose (HFr)] or glucose-sweetened [high glucose (HGI)] beverage. Meals were isocaloric in the two treatments. Postprandial glycemic excursions were reduced by 66 ± 12%, and insulin responses were 65 ± 5% lower (both P < 0.001) during HFr consumption. The area under the curve for leptin during the first 12 h (-33 ± 7%; P < 0.005), the entire 24 h (-21 ± 8%; P < 0.02), and the diurnal amplitude (peak - nadir) (24 ± 6%; P < 0.0025) were reduced on the HFr day compared with the HGI day. In addition, circulating levels of the orexigenic gastroenteric hormone, ghrelin, were suppressed by approximately 30% 1-2 h after ingestion of each HGI meal (P < 0.01), but postprandial suppression of ghrelin was significantly less pronounced after HFr meals (P < 0.05 vs. HGI). Consumption of HFr meals produced a rapid and prolonged elevation of plasma triglycérides compared with the HGI day (P < 0.005). Because insulin and leptin, and possibly ghrelin, function as key signals to the central nervous system in the long-term regulation of energy balance, decreases of circulating insulin and leptin and increased ghrelin concentrations, as demonstrated in this study, could lead to increased caloric intake and ultimately contribute to weight gain and obesity during chronic consumption of diets high in fructose.

Original languageEnglish (US)
Pages (from-to)2963-2972
Number of pages10
JournalJournal of Clinical Endocrinology and Metabolism
Volume89
Issue number6
DOIs
StatePublished - Jun 2004

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Ghrelin
Leptin
Fructose
Triglycerides
Insulin
Meals
Glucose
Beverages
Neurology
Nutrition
Energy Intake
Energy balance
Metabolism
Weight Gain
Area Under Curve
Blood
Central Nervous System
Obesity
Eating
Fats

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology, Diabetes and Metabolism

Cite this

Dietary fructose reduces circulating insulin and leptin, attenuates postprandial suppression of ghrelin, and increases triglycerides in women. / Teff, Karen L.; Elliott, Sharon S.; Tschöp, Matthias; Kieffer, Timothy J.; Rader, Daniel; Heiman, Mark; Townsend, Raymond R.; Keim, Nancy L.; D'Alessio, David; Havel, Peter J.

In: Journal of Clinical Endocrinology and Metabolism, Vol. 89, No. 6, 06.2004, p. 2963-2972.

Research output: Contribution to journalArticle

Teff, Karen L. ; Elliott, Sharon S. ; Tschöp, Matthias ; Kieffer, Timothy J. ; Rader, Daniel ; Heiman, Mark ; Townsend, Raymond R. ; Keim, Nancy L. ; D'Alessio, David ; Havel, Peter J. / Dietary fructose reduces circulating insulin and leptin, attenuates postprandial suppression of ghrelin, and increases triglycerides in women. In: Journal of Clinical Endocrinology and Metabolism. 2004 ; Vol. 89, No. 6. pp. 2963-2972.
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T1 - Dietary fructose reduces circulating insulin and leptin, attenuates postprandial suppression of ghrelin, and increases triglycerides in women

AU - Teff, Karen L.

AU - Elliott, Sharon S.

AU - Tschöp, Matthias

AU - Kieffer, Timothy J.

AU - Rader, Daniel

AU - Heiman, Mark

AU - Townsend, Raymond R.

AU - Keim, Nancy L.

AU - D'Alessio, David

AU - Havel, Peter J

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N2 - Previous studies indicate that leptin secretion is regulated by insulin-mediated glucose metabolism. Because fructose, unlike glucose, does not stimulate insulin secretion, we hypothesized that meals high in fructose would result in lower leptin concentrations than meals containing the same amount of glucose. Blood samples were collected every 30-60 min for 24 h from 12 normal-weight women on 2 randomized days during which the subjects consumed three meals containing 55, 30, and 15% of total kilocalories as carbohydrate, fat, and protein, respectively, with 30% of kilocalories as either a fructose-sweetened [high fructose (HFr)] or glucose-sweetened [high glucose (HGI)] beverage. Meals were isocaloric in the two treatments. Postprandial glycemic excursions were reduced by 66 ± 12%, and insulin responses were 65 ± 5% lower (both P < 0.001) during HFr consumption. The area under the curve for leptin during the first 12 h (-33 ± 7%; P < 0.005), the entire 24 h (-21 ± 8%; P < 0.02), and the diurnal amplitude (peak - nadir) (24 ± 6%; P < 0.0025) were reduced on the HFr day compared with the HGI day. In addition, circulating levels of the orexigenic gastroenteric hormone, ghrelin, were suppressed by approximately 30% 1-2 h after ingestion of each HGI meal (P < 0.01), but postprandial suppression of ghrelin was significantly less pronounced after HFr meals (P < 0.05 vs. HGI). Consumption of HFr meals produced a rapid and prolonged elevation of plasma triglycérides compared with the HGI day (P < 0.005). Because insulin and leptin, and possibly ghrelin, function as key signals to the central nervous system in the long-term regulation of energy balance, decreases of circulating insulin and leptin and increased ghrelin concentrations, as demonstrated in this study, could lead to increased caloric intake and ultimately contribute to weight gain and obesity during chronic consumption of diets high in fructose.

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