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Review Articles

The consequence and mechanism of dietary flavonoids on androgen profiles and disorders amelioration

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Pages 11327-11350 | Published online: 07 Jul 2022
 

Abstract

Androgen is a kind of steroid hormone that plays a vital role in reproductive system and homeostasis of the body. Disrupted androgen balance serves as the causal contributor to a series of physiological disorders and even diseases. Flavonoids, as an extremely frequent family of natural polyphenols, exist widely in plants and foods and have received great attention when considering their inevitable consumption and estrogen-like effects. Mounting evidence illustrates that flavonoids have a propensity to interfere with androgen synthesis and metabolism, and also have a designated improvement effect on androgen disorders. Therefore, flavonoids were divided into six subclasses based on the structural feature in this paper, and the literature about their effects on androgens published in the past ten years was summarized. It could be concluded that flavonoids have the potential to regulate androgen levels and biological effects, mainly by interfering with the hypothalamic-pituitary-gonadal axis, androgen synthesis and metabolism, androgen binding with its receptors and membrane receptors, and antioxidant effects. The faced challenges about androgen regulation by flavonoids masterly include target mechanism exploration, individual heterogeneity, food matrixes interaction, and lack of clinical study. This review also provides a scientific basis for nutritional intervention using flavonoids to improve androgen disorder symptoms.

Disclosure statement

The authors declare no conflict of interest.

Abbreviations

1,3-DCP=

1,3-dichloro-2-propanol

11OH-A4=

11OH-androstenedione

17β-HSD=

17β-hydroxysteroid dehydrogenase

3-MCPD=

3-Chloro-1,2-propanediol

3β-HSD=

3β-hydroxysteroid dehydrogenase

AMPK=

adenosine 5-monophosphate-activated protein kinase

AD=

androgen deficiency

AR=

androgen receptor

A4=

Androstenedione

BPH=

benign prostatic hyperplasia

Cd=

cadmium

CYP11A1=

cytochrome P450 cholesterol side-chain cleavage

C3G=

cyanidin-3-O-glucoside

cAMP=

cyclic adenosine monophosphate

CYP17A1=

cytochrome P450 17α-hydroxylase/17,20-lyase

DHEA=

Dehydroepiandrosterone

DHEAS=

dehydroepiandrosterone sulfate

DEHP=

di-(2-ethylhexyl) phthalate

DHT=

Dihydrotestosterone

EDCs=

endocrine-disrupting compounds

EGCG=

epigallocatechin gallate

E2=

estradiol

Fdx1=

ferredoxin1

FSH=

follicle-stimulating hormone

FSHR=

follicle-stimulating hormone receptor

GnRH=

gonadotropin-releasing hormone

GPRC6A=

G Protein-coupled receptor family C group 6 member A

GA=

gallic acid

GATA1=

GATA-binding factor 1

IC50=

half-maximal inhibition

HAART=

Highly active antiretroviral therapy

HPG=

hypothalamic-pituitary-gonadal

LH=

luteinizing hormone

LHR=

luteinizing hormone receptor

MMPs=

matrix metalloproteinases

NAFLD=

nonalcoholic fatty liver disease

PI3K=

phosphatidylinositol 3-kinase

PCOS=

polycystic ovary syndrome

PREG=

pregnenolone

PROG=

progesterone

PCa=

prostate cancer

PKA=

protein kinase A

PCA=

protocatechuic acid

RoDH2=

retinol dehydrogenase 2

SRD5A=

steroid 5α-reductase

StAR=

steroidogenic acute response protein

SULT=

sulfotransferase

UGTs=

uridine diphosphate-glucuronosyl transferase

uPAR=

urokinase plasminogen activator receptors

ZIP9=

zinc transporter member 9

Additional information

Funding

This work was supported by the National Natural Science Foundation of China (NO. 32172220) and the Youth Science and Technology Innovation Talent of Guangdong TeZhi Plan (2019TQ05N770). The authors also thank the Guangdong Key Area Research and Development Program (NO. 2019B020210003), the Science and Technology Program of Guangzhou (NO. 202206010121), and the Fundamental Research Funds for the Central Universities (NO. 21622108).

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