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Carotenoids in Adipose Tissue Biology and Obesity

Chapter
First Online:
Part of the Subcellular Biochemistry book series (SCBI, volume 79)

Abstract

Cell, animal and human studies dealing with carotenoids and carotenoid derivatives as nutritional regulators of adipose tissue biology with implications for the etiology and management of obesity and obesity-related metabolic diseases are reviewed. Most studied carotenoids in this context are β-carotene, cryptoxanthin, astaxanthin and fucoxanthin, together with β-carotene-derived retinoids and some other apocarotenoids. Studies indicate an impact of these compounds on essential aspects of adipose tissue biology including the control of adipocyte differentiation (adipogenesis), adipocyte metabolism, oxidative stress and the production of adipose tissue-derived regulatory signals and inflammatory mediators. Specific carotenoids and carotenoid derivatives restrain adipogenesis and adipocyte hypertrophy while enhancing fat oxidation and energy dissipation in brown and white adipocytes, and counteract obesity in animal models. Intake, blood levels and adipocyte content of carotenoids are reduced in human obesity. Specifically designed human intervention studies in the field, though still sparse, indicate a beneficial effect of carotenoid supplementation in the accrual of abdominal adiposity. In summary, studies support a role of specific carotenoids and carotenoid derivatives in the prevention of excess adiposity, and suggest that carotenoid requirements may be dependent on body composition.

Keywords

Carotenoids Apocarotenoids Retinoids Vitamin A metabolism Obesity Adiposity Energy metabolism White adipose tissue browning Human epidemiological studies 

Abbreviations

ADH

alcohol dehydrogenase

ALDH

aldehyde dehydrogenase

AMPK

AMP-dependent protein kinase

atRA

all trans retinoic acid

BAT

brown adipose tissue

BC

β-carotene

BCO1

β-carotene-15,15′-oxygenase

BCO2

β-carotene-9’,10′-oxygenase

BMI

body mass index

bw

body weight

C/EBP

CCAAT-enhancer binding protein

CD36

cluster of differentiation 36

CRABP

cellular retinoic acid binding protein

CRBP

cellular retinol binding protein

FABP

fatty acid binding protein

ISX

intestine-specific homeobox

LRAT

lecithin: retinol acyltransferase

LDLr

low density lipoprotein receptor

LPL

lipoprotein lipase

NF-κB

nuclear factor κB

Nrf2

nuclear factor erythroid 2-related factor 2

PPAR

peroxisome proliferator activated receptor

Rald

retinaldehyde

RAR

retinoic acid receptor

RBP (or RBP4)

retinol binding protein

RBPR2

RBP receptor 2

RDH

retinol dehydrogenase

REH

retinyl ester hydrolase

ROS

reactive oxygen species

RXR

retinoid X receptor

SR-B1

scavenger receptor class B, member 1

STRA6

stimulated retinoic acid 6

UCP1

uncoupling protein 1

WAT

white adipose.

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Notes

Acknowledgements

The authors acknowledge funding support from the European Union’s Seventh Framework Programme FP7 under grant agreements n. 244995 (BIOCLAIMS Project) and n. 278373 (DIABAT project), the Spanish Government (grant AGL2012-33692), Fundación Ramón Areces, and the Instituto de Salud Carlos III, Centro de Investigación Biomédica en Red Fisiopatología de la Obesidad y Nutrición, CIBERobn. The authors are also grateful to The Nemours Research Foundation and The Players Center for Child Health at Wolfson Children’s Hospital in Jacksonville, Florida for their generous support. The UIB group is a member of the European Nutrigenomics Organization and the network IBERCAROT (CYTED, Spanish Government, n° 112RT0445).

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© Springer International Publishing Switzerland 2016

Authors and Affiliations

  1. 1.Group of Nutrigenomics and Obesity, Laboratory of Molecular Biology, Nutrition and BiotechnologyUniversitat de les Illes BalearsPalma de MallorcaSpain
  2. 2.CIBER Fisiopatología de la Obesidad y Nutrición (CIBERobn)Palma de MallorcaSpain
  3. 3.Metabolism and DiabetesNemours Children’s ClinicJacksonvilleUSA

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