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Raspberry seed flour attenuates high-sucrose diet-mediated hepatic stress and adipose tissue inflammation.

The Journal of nutritional biochemistry
June 1, 2016
Inhae Kang et al. (5 authors)
Comparative StudyJournal ArticleResearch Support, U.S. Gov't, Non-P.H.S.Human StudyAnimal StudyMolecular Study
Study Details

Study Goal

The researchers aimed to determine whether ellagic acid (EA) supplementation could mitigate high-sucrose diet-induced hepatic toxicity and metabolic dysregulation.

Results Summary

EA supplementation improved dyslipidemia, restored glucose homeostasis, reduced hepatic ER stress and oxidative damage, and decreased visceral adipocyte hypertrophy and adipose tissue inflammation.

Population

C57BL/6 male mice and human hepatoma cells.

Effective Dosage

Equivalent to 0.03% of EA from raspberry seed flour.

Duration

12 weeks.

Interactions

None mentioned.

Extracted Claims (12)
InterventionDirectionEndpointPopulationDosageImpactClaim #
Chronic intake of high sucrose (HS) diet
increase
high-fat (HF) diet-induced obesity and its associated metabolic complications
-
-
exacerbates
#1
ellagic acid (EA)
decrease
lipid levels
hepatocytes and adipocytes
-
exerts distinct lipid-lowering characteristics
#2
EA supplementation
decrease
HS diet-mediated hepatic toxicity and its accompanied metabolic dysregulation
-
-
inhibits
#3
EA from RSF
decrease
HFHS diet-mediated dyslipidemia
C57BL/6 male mice
-
significantly improved
#4
EA from RSF
increase
glucose homeostasis levels
C57BL/6 male mice
similar to the HF diet-fed mice
restored
#5
EA
decrease
activation of endoplasmic reticulum (ER) stress and oxidative damage triggered by HFHS diet in the liver
C57BL/6 male mice
-
substantially reversed
#6
EA
decrease
ER stress and reactive oxygen species (ROS) production
human hepatoma cells
-
reducing
#7
HFHS-R diet
decrease
visceral adipocyte hypertrophy and adipose tissue inflammation
C57BL/6 male mice
-
significantly decreased
#8
HFHS-R diet
decrease
proinflammatory gene expression and macrophage infiltration
C57BL/6 male mice
-
reduced
#9
EA supplementation from RSF
decrease
HFHS diet-mediated metabolic complication
-
-
effective in reducing
#10
EA supplementation from RSF
decrease
hepatic ER and oxidative stresses as well as adipocyte inflammation
-
-
attenuating
#11
inclusion of EA in diets
decrease
metabolic insults triggered by HS consumption
-
-
may normalize
#12
Abstract

Chronic intake of high sucrose (HS) diet exacerbates high-fat (HF) diet-induced obesity and its associated metabolic complications. Previously, we have demonstrated that ellagic acid (EA), an abundant polyphenol found in some fruits and nuts, exerts distinct lipid-lowering characteristics in hepatocytes and adipocytes. In this study, we hypothesized that EA supplementation inhibits HS diet-mediated hepatic toxicity and its accompanied metabolic dysregulation. To test this hypothesis, C57BL/6 male mice were randomly assigned to three isocaloric HF diets (41% calories from fat) containing either no-sucrose (HF), high-sucrose (HFHS), or high-sucrose plus EA (HFHS-R) from raspberry seed flour (RSF, equivalent to 0.03% of EA), and fed for 12weeks. The inclusion of EA from RSF significantly improved HFHS diet-mediated dyslipidemia and restored glucose homeostasis levels similar to the HF diet-fed mice. Despite marginal difference in hepatic triglyceride content, the addition of EA substantially reversed the activation of endoplasmic reticulum (ER) stress and oxidative damage triggered by HFHS diet in the liver. These effects of EA were further confirmed in human hepatoma cells by reducing ER stress and reactive oxygen species (ROS) production. Moreover, HFHS-R diet significantly decreased visceral adipocyte hypertrophy and adipose tissue inflammation evidenced by reduced proinflammatory gene expression and macrophage infiltration. In summary, EA supplementation from RSF was effective in reducing HFHS diet-mediated metabolic complication by attenuating hepatic ER and oxidative stresses as well as adipocyte inflammation. Our results suggest that the inclusion of EA in diets may normalize metabolic insults triggered by HS consumption.

Medical Subject Headings (MeSH)
AdiposityAnimalsAnti-Inflammatory Agents, Non-SteroidalAntioxidantsBiomarkersCell Line, TumorDiet, Carbohydrate LoadingDiet, High-FatDietary SucroseDietary SupplementsEllagic AcidEndoplasmic Reticulum StressHumansIntra-Abdominal FatLiverMaleMice, Inbred C57BLObesityOxidative StressPanniculitisRandom AllocationRubusSeedsSpecific Pathogen-Free Organisms
Study Links
Quality Scores
SafetyNot Assessed
Efficacy85/10
Quality78/10
Citation Metrics
Total Citations37
Citations/Year4.1
Relative Citation Ratio1.75
NIH Percentile70.4%
Research Impact Scores
APT Score0.50
Weight Score0.96
Normalized Score0.70
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