The relation between dietary fructose, dietary fat and leptin responsiveness in rats

Samantha J. Haring, Ruth Babette Harris

Research output: Contribution to journalArticle

26 Citations (Scopus)

Abstract

Others reported that rats fed a high-fructose diet for 6. months were leptin resistant. We tested peripheral and/or central leptin responses in rats fed fructose for shorter time periods. Rats fed a diet containing 60% energy (%. kcal) fructose and 10%. kcal fat diet for 21. days had the same serum triglycerides (TG), gained less weight than controls, decreased their food intake and weight gain in response to central injections of 0.5 or 1.0. ug leptin, but were resistant to an i.p. injection of 2.0. mg. leptin/kg. An i.p. injection of 1. mg. leptin/kg increased phosphorylation of hypothalamic signal transducer and activator of transcription 3 (PSTAT3) implying resistance was not a failure of leptin to cross the blood brain barrier. The effects of dietary fructose were compared with those of dietary fat. Rats fed a 10%. kcal fructose and 30%. kcal fat diet for 39. days were leptin resistant whereas rats fed a 40%. kcal fructose and 30%. kcal fat diet responded to i.p. leptin. Another monosaccharide, glucose, replicated the effects of fructose in the 30%. kcal fat diet. Surprisingly, none of the rats showed a reliable response to third ventricle leptin and peripheral leptin failed to stimulate hypothalamic PSTAT3 although it did increase PSTAT3 in the brainstem of rats fed the 40%. kcal fructose or glucose diets. Thus a high-fructose, low-fat diet induces peripheral leptin resistance in less than 4. weeks, but high dietary concentrations of fructose or glucose prevent peripheral leptin resistance in rats fed a high-fat diet.

Original languageEnglish (US)
Pages (from-to)914-922
Number of pages9
JournalPhysiology and Behavior
Volume104
Issue number5
DOIs
StatePublished - Oct 24 2011

Fingerprint

Dietary Fats
Leptin
Fructose
Diet
STAT3 Transcription Factor
Fats
Phosphorylation
Glucose
Vascular Resistance
Injections
Fat-Restricted Diet
Third Ventricle
Monosaccharides
High Fat Diet
Blood-Brain Barrier
Brain Stem
Weight Gain
Triglycerides
Eating

Keywords

  • Dietary fat
  • Food intake
  • STAT3
  • Triglycerides
  • Weight gain

ASJC Scopus subject areas

  • Experimental and Cognitive Psychology
  • Behavioral Neuroscience

Cite this

The relation between dietary fructose, dietary fat and leptin responsiveness in rats. / Haring, Samantha J.; Harris, Ruth Babette.

In: Physiology and Behavior, Vol. 104, No. 5, 24.10.2011, p. 914-922.

Research output: Contribution to journalArticle

@article{ae8cc4f68f4b4b0ab994e187ce229a31,
title = "The relation between dietary fructose, dietary fat and leptin responsiveness in rats",
abstract = "Others reported that rats fed a high-fructose diet for 6. months were leptin resistant. We tested peripheral and/or central leptin responses in rats fed fructose for shorter time periods. Rats fed a diet containing 60{\%} energy ({\%}. kcal) fructose and 10{\%}. kcal fat diet for 21. days had the same serum triglycerides (TG), gained less weight than controls, decreased their food intake and weight gain in response to central injections of 0.5 or 1.0. ug leptin, but were resistant to an i.p. injection of 2.0. mg. leptin/kg. An i.p. injection of 1. mg. leptin/kg increased phosphorylation of hypothalamic signal transducer and activator of transcription 3 (PSTAT3) implying resistance was not a failure of leptin to cross the blood brain barrier. The effects of dietary fructose were compared with those of dietary fat. Rats fed a 10{\%}. kcal fructose and 30{\%}. kcal fat diet for 39. days were leptin resistant whereas rats fed a 40{\%}. kcal fructose and 30{\%}. kcal fat diet responded to i.p. leptin. Another monosaccharide, glucose, replicated the effects of fructose in the 30{\%}. kcal fat diet. Surprisingly, none of the rats showed a reliable response to third ventricle leptin and peripheral leptin failed to stimulate hypothalamic PSTAT3 although it did increase PSTAT3 in the brainstem of rats fed the 40{\%}. kcal fructose or glucose diets. Thus a high-fructose, low-fat diet induces peripheral leptin resistance in less than 4. weeks, but high dietary concentrations of fructose or glucose prevent peripheral leptin resistance in rats fed a high-fat diet.",
keywords = "Dietary fat, Food intake, STAT3, Triglycerides, Weight gain",
author = "Haring, {Samantha J.} and Harris, {Ruth Babette}",
year = "2011",
month = "10",
day = "24",
doi = "10.1016/j.physbeh.2011.05.032",
language = "English (US)",
volume = "104",
pages = "914--922",
journal = "Physiology and Behavior",
issn = "0031-9384",
publisher = "Elsevier Inc.",
number = "5",

}

TY - JOUR

T1 - The relation between dietary fructose, dietary fat and leptin responsiveness in rats

AU - Haring, Samantha J.

AU - Harris, Ruth Babette

PY - 2011/10/24

Y1 - 2011/10/24

N2 - Others reported that rats fed a high-fructose diet for 6. months were leptin resistant. We tested peripheral and/or central leptin responses in rats fed fructose for shorter time periods. Rats fed a diet containing 60% energy (%. kcal) fructose and 10%. kcal fat diet for 21. days had the same serum triglycerides (TG), gained less weight than controls, decreased their food intake and weight gain in response to central injections of 0.5 or 1.0. ug leptin, but were resistant to an i.p. injection of 2.0. mg. leptin/kg. An i.p. injection of 1. mg. leptin/kg increased phosphorylation of hypothalamic signal transducer and activator of transcription 3 (PSTAT3) implying resistance was not a failure of leptin to cross the blood brain barrier. The effects of dietary fructose were compared with those of dietary fat. Rats fed a 10%. kcal fructose and 30%. kcal fat diet for 39. days were leptin resistant whereas rats fed a 40%. kcal fructose and 30%. kcal fat diet responded to i.p. leptin. Another monosaccharide, glucose, replicated the effects of fructose in the 30%. kcal fat diet. Surprisingly, none of the rats showed a reliable response to third ventricle leptin and peripheral leptin failed to stimulate hypothalamic PSTAT3 although it did increase PSTAT3 in the brainstem of rats fed the 40%. kcal fructose or glucose diets. Thus a high-fructose, low-fat diet induces peripheral leptin resistance in less than 4. weeks, but high dietary concentrations of fructose or glucose prevent peripheral leptin resistance in rats fed a high-fat diet.

AB - Others reported that rats fed a high-fructose diet for 6. months were leptin resistant. We tested peripheral and/or central leptin responses in rats fed fructose for shorter time periods. Rats fed a diet containing 60% energy (%. kcal) fructose and 10%. kcal fat diet for 21. days had the same serum triglycerides (TG), gained less weight than controls, decreased their food intake and weight gain in response to central injections of 0.5 or 1.0. ug leptin, but were resistant to an i.p. injection of 2.0. mg. leptin/kg. An i.p. injection of 1. mg. leptin/kg increased phosphorylation of hypothalamic signal transducer and activator of transcription 3 (PSTAT3) implying resistance was not a failure of leptin to cross the blood brain barrier. The effects of dietary fructose were compared with those of dietary fat. Rats fed a 10%. kcal fructose and 30%. kcal fat diet for 39. days were leptin resistant whereas rats fed a 40%. kcal fructose and 30%. kcal fat diet responded to i.p. leptin. Another monosaccharide, glucose, replicated the effects of fructose in the 30%. kcal fat diet. Surprisingly, none of the rats showed a reliable response to third ventricle leptin and peripheral leptin failed to stimulate hypothalamic PSTAT3 although it did increase PSTAT3 in the brainstem of rats fed the 40%. kcal fructose or glucose diets. Thus a high-fructose, low-fat diet induces peripheral leptin resistance in less than 4. weeks, but high dietary concentrations of fructose or glucose prevent peripheral leptin resistance in rats fed a high-fat diet.

KW - Dietary fat

KW - Food intake

KW - STAT3

KW - Triglycerides

KW - Weight gain

UR - http://www.scopus.com/inward/record.url?scp=80053052166&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=80053052166&partnerID=8YFLogxK

U2 - 10.1016/j.physbeh.2011.05.032

DO - 10.1016/j.physbeh.2011.05.032

M3 - Article

C2 - 21684298

AN - SCOPUS:80053052166

VL - 104

SP - 914

EP - 922

JO - Physiology and Behavior

JF - Physiology and Behavior

SN - 0031-9384

IS - 5

ER -