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Dietary Polyphenols and Obesity: A Review of Polyphenol Effects on Lipid and Glucose Metabolism, Mitochondrial Homeostasis, and Starch Digestibility and Absorption

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Abstract

Obesity is a major global public health concern, limiting socio-economic development and human productivity. As studies focus on finding sustainable solutions to this challenge, polyphenols have shown promising results and have become a research focus. This is mainly because of associated lower risks of side effects with their use, compared to synthetic pharmaceuticals. In this study, the anti-obesity potentials of dietary polyphenols have been reviewed. Using a narrative approach, the biological activities of polyphenols and their influence on energy metabolism and mechanisms are discussed. Specifically, their roles in insulin-dependent glucose uptake, insulin sensitivity, lipid metabolism and storage in adipocytes, starch digestibility, and regulation of mitophagy and mitogenesis in muscle cells and adipocytes, were considered. After considering the major findings of many related studies, it was confirmed that polyphenols can prevent and ameliorate obesity by fighting insulin resistance (IR) induced by pro-inflammatory cytokines, scavenging reactive oxygen species (ROS) and limiting their effects, and by regulating the expression and/or activity of key enzymes along relevant pathways. More human studies are needed to reveal more about the anti-obesity effects of dietary polyphenols and their effective doses in humans.

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Data Availability

Data sharing not applicable to this article as no datasets were generated or analysed during the current study.

Abbreviations

IR:

Insulin resistance

ROS:

Reactive oxygen species

EGCG:

Epigallocatechin-3-O-gallate

RSV:

Resveratrol

GA:

Gallic acid

CRC:

Curcumin

IS:

Insulin sensitivity

CR:

Caloric restriction

GLUT:

Glucose transporter

GSV:

Glucose transporter storage vesicle

NF-kB:

Nuclear factor kappa B

JNK:

C-Jun N-terminal kinase

SFA:

Saturated fatty acid

TNF α:

Tumor necrosis factor alpha

NADPH:

Reduced nicotinamide adenine dinucleotide phosphate

NOX:

NADPH oxidase

IRS-1:

Insulin receptor substrate 1

PI3K:

Phosphatidylinositol-3-kinase

Akt:

Collective name of a set of three serine/threonine-specific protein kinases

NO:

Nitric oxide

eNOS:

Endothelial NO synthase

mTOR:

Mammalian target of rapamycin

HepG2:

Human liver cells

IR-HepG2:

Insulin resistant human liver cells

PEPCK:

Phosphoenolpyruvate carboxykinase

G6Pase:

Glucose-6-phosphatase

LDL:

Low density lipoprotein

HDL:

High density lipoprotein

RGPD:

Red grape pomace drink

AMPK:

AMP-activated protein kinase

PTB1B:

Protein tyrosine phosphatase 1B

LKB1:

Liver kinase B1

CaMKK:

Calcium/calmodulin-dependent protein kinase kinase

RA:

Rosmarinic acid

IGF-1:

Insulin-like growth factor 1

SREBP:

Sterol regulatory-element binding proteins

PPAR:

Peroxisome proliferator-activated receptors

G3P:

Glyceraldehyde 3-phosphate

GPDH:

Glycerol-3-phosphate dehydrogenase

HMG-CoA:

3-Hydroxy-3-methylglutaryl coenzyme A

FABP4:

Fatty acid binding protein 4

LXR-α:

Liver X receptor alpha

PGC-1:

Peroxisome proliferator-activated receptor-gamma coactivator-1alpha

Ucpl:

Uncoupling protein 1

CIDEA:

Cell death-inducing DNA fragmentation factor alpha-like effector A

Tbx1:

Tata-box protein 1

Cd137:

Tumor necrosis factor receptor superfamily member 9

BAT:

Beige adipose tissue

iWAT:

Inguinal white adipose tissues

SIRT1:

Sirtuin 1

SCD 1:

Stearoyl-Coenzyme A desaturase 1

ATP:

Adenosine triphosphate

NAD:

Nicotinamide adenine dinucleotide

FOXO3:

Forkhead box O3

UNC51:

Autophagy-related serine/threonine kinase

ULK1:

UNC-51-like kinase 1

PINK 1:

PTEN induced putative kinase 1

PTEN:

A tumor suppressor phosphatase and tensin homolog

ERK2:

Mitogen-activated protein kinase 1 (MAPK1)

NAMPT:

Nicotinamide phosphoribosyltransferase

PKD:

Protein kinase D

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Author notes

  1. David Asante-Donyinah, Emmanuel Letsyo, John Dzikunoo and Zeenatu Suglo Adams contributed equally to this work.

Authors and Affiliations

  1. Department of Food Science and Technology, Faculty of Applied Sciences and Technology, Ho Technical University, P.O. Box HP217, Ho, Volta Region, Ghana

    Courage Sedem Dzah, David Asante-Donyinah, Emmanuel Letsyo, John Dzikunoo & Zeenatu Suglo Adams

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  1. Courage Sedem Dzah
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  2. David Asante-Donyinah
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Courage Sedem Dzah conceptualized the study, drafted some sections, did the editing of the manuscript and finalized the paper. Emmanuel Letsyo and John Dzikunoo also drafted some sections of the paper and helped with proofreading, David Asante-Donyinah and Zeenatu Sugloh Adams contributed by drafting some sections of the paper. All authors read and approved the final version of the manuscript for submission.

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Correspondence to Courage Sedem Dzah.

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Dzah, C.S., Asante-Donyinah, D., Letsyo, E. et al. Dietary Polyphenols and Obesity: A Review of Polyphenol Effects on Lipid and Glucose Metabolism, Mitochondrial Homeostasis, and Starch Digestibility and Absorption. Plant Foods Hum Nutr 78, 1–12 (2023). https://doi.org/10.1007/s11130-022-01034-6

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