Responses of inflammatory markers to a low-fat, high-carbohydrate diet: Effects of energy intake

Siddika E Karakas, Alex Tsodikov, Uma Singh, Ishwaral Jialal

Research output: Contribution to journalArticle

59 Citations (Scopus)

Abstract

Background: Inflammation contributes to atherogenesis. Dietary fats may be proinflammatory. Objective: The objective was to determine whether energy intake modulates the effects of low-fat, high-carbohydrate intakes on inflammatory markers. Design: Twenty-two healthy postmenopausal women with a mean (±SD) age of 61 ± 11 y, who were not receiving hormone replacement therapy, were fed eucaloric diets to reduce their fat intake from 35% to 15% of energy. Next, the women consumed a 15%-fat ad libitum diet under free-living conditions. Serum highly sensitive C-reactive protein, interleukin 6, HDL serum amyloid A, and adiponectin concentrations were measured at the end of the eucaloric and ad libitum low-fat, high-carbohydrate intakes. Results: The eucaloric diet decreased adiponectin from 16.3 ± 2.1 to 14.2 ± 2.0 mg/L (P < 0.05) and increased triacylglycerol from 131 ± 11 to 164 ± 14 mg/dL (P < 0.01). The ad libitum low-fat diet caused 6 kg weight loss and decreased highly sensitive C-reactive protein from 4.3 ± 0.6 to 2.5 ± 0.5 mg/L (P < 0.01), decreased HDL serum amyloid A from 10.3 ± 1.8 to 5.7 ± 1.3 mg/L (P < 0.001), increased adiponectin from 14.2 ± 2.0 to 16.3 ± 1.7 mg/L (P < 0.05), and decreased triacylglycerol from 164 ± 14 to 137 ± 15 mg/dL (P < 0.05). Conclusion: During the eucaloric phase, the low-fat, high-carbohydrate diet exerted unfavorable effects on the inflammatory markers. In contrast, the ad libitum low-fat, high-carbohydrate intake caused weight loss and affected inflammatory markers favorably. Thus, the energy content of a low-fat, high-carbohydrate diet determines changes in inflammatory markers.

Original languageEnglish (US)
Pages (from-to)774-779
Number of pages6
JournalAmerican Journal of Clinical Nutrition
Volume83
Issue number4
StatePublished - Apr 1 2006

Fingerprint

high carbohydrate diet
High Fat Diet
Energy Intake
energy intake
inflammation
Fats
Carbohydrates
Adiponectin
adiponectin
carbohydrate intake
Serum Amyloid A Protein
lipids
Diet
C-Reactive Protein
C-reactive protein
amyloid
Weight Loss
Triglycerides
weight loss
triacylglycerols

Keywords

  • Energy intake
  • Inflammatory markers
  • Low-fat diet
  • Weight loss

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Food Science

Cite this

Responses of inflammatory markers to a low-fat, high-carbohydrate diet : Effects of energy intake. / Karakas, Siddika E; Tsodikov, Alex; Singh, Uma; Jialal, Ishwaral.

In: American Journal of Clinical Nutrition, Vol. 83, No. 4, 01.04.2006, p. 774-779.

Research output: Contribution to journalArticle

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N2 - Background: Inflammation contributes to atherogenesis. Dietary fats may be proinflammatory. Objective: The objective was to determine whether energy intake modulates the effects of low-fat, high-carbohydrate intakes on inflammatory markers. Design: Twenty-two healthy postmenopausal women with a mean (±SD) age of 61 ± 11 y, who were not receiving hormone replacement therapy, were fed eucaloric diets to reduce their fat intake from 35% to 15% of energy. Next, the women consumed a 15%-fat ad libitum diet under free-living conditions. Serum highly sensitive C-reactive protein, interleukin 6, HDL serum amyloid A, and adiponectin concentrations were measured at the end of the eucaloric and ad libitum low-fat, high-carbohydrate intakes. Results: The eucaloric diet decreased adiponectin from 16.3 ± 2.1 to 14.2 ± 2.0 mg/L (P < 0.05) and increased triacylglycerol from 131 ± 11 to 164 ± 14 mg/dL (P < 0.01). The ad libitum low-fat diet caused 6 kg weight loss and decreased highly sensitive C-reactive protein from 4.3 ± 0.6 to 2.5 ± 0.5 mg/L (P < 0.01), decreased HDL serum amyloid A from 10.3 ± 1.8 to 5.7 ± 1.3 mg/L (P < 0.001), increased adiponectin from 14.2 ± 2.0 to 16.3 ± 1.7 mg/L (P < 0.05), and decreased triacylglycerol from 164 ± 14 to 137 ± 15 mg/dL (P < 0.05). Conclusion: During the eucaloric phase, the low-fat, high-carbohydrate diet exerted unfavorable effects on the inflammatory markers. In contrast, the ad libitum low-fat, high-carbohydrate intake caused weight loss and affected inflammatory markers favorably. Thus, the energy content of a low-fat, high-carbohydrate diet determines changes in inflammatory markers.

AB - Background: Inflammation contributes to atherogenesis. Dietary fats may be proinflammatory. Objective: The objective was to determine whether energy intake modulates the effects of low-fat, high-carbohydrate intakes on inflammatory markers. Design: Twenty-two healthy postmenopausal women with a mean (±SD) age of 61 ± 11 y, who were not receiving hormone replacement therapy, were fed eucaloric diets to reduce their fat intake from 35% to 15% of energy. Next, the women consumed a 15%-fat ad libitum diet under free-living conditions. Serum highly sensitive C-reactive protein, interleukin 6, HDL serum amyloid A, and adiponectin concentrations were measured at the end of the eucaloric and ad libitum low-fat, high-carbohydrate intakes. Results: The eucaloric diet decreased adiponectin from 16.3 ± 2.1 to 14.2 ± 2.0 mg/L (P < 0.05) and increased triacylglycerol from 131 ± 11 to 164 ± 14 mg/dL (P < 0.01). The ad libitum low-fat diet caused 6 kg weight loss and decreased highly sensitive C-reactive protein from 4.3 ± 0.6 to 2.5 ± 0.5 mg/L (P < 0.01), decreased HDL serum amyloid A from 10.3 ± 1.8 to 5.7 ± 1.3 mg/L (P < 0.001), increased adiponectin from 14.2 ± 2.0 to 16.3 ± 1.7 mg/L (P < 0.05), and decreased triacylglycerol from 164 ± 14 to 137 ± 15 mg/dL (P < 0.05). Conclusion: During the eucaloric phase, the low-fat, high-carbohydrate diet exerted unfavorable effects on the inflammatory markers. In contrast, the ad libitum low-fat, high-carbohydrate intake caused weight loss and affected inflammatory markers favorably. Thus, the energy content of a low-fat, high-carbohydrate diet determines changes in inflammatory markers.

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KW - Low-fat diet

KW - Weight loss

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