Maternal Supplementation with β-Carotene During Pregnancy Disturbs Lipid Metabolism and Glucose Homoeostasis in F1 Female Mice

Molecular Nutrition & Food Research
Jiaojiao GuoChonggang Wang

Abstract

β-Carotene (BC), a substitute for vitamin A, is widely used for its benefits. The present study investigates whether in-utero BC administration can alter lipid and glucose homoeostasis in offspring. Pregnant mice are supplemented with BC (1 mg kg-1 weight) by oral gavage once every 3 days, for a total of six doses. Increased visceral fat may be caused by up-regulated PPARγ (peroxisome proliferator-activated receptor gamma) and RXRα/β (retinoid X receptors) in liver and adipose tissue, and glucose intolerance is observed in F1 adult females prenatally supplemented with BC, while F1 males do not exhibit these symptoms. In females, increased serum leptin, resistin, and IL-6 and reduced adiponectin, caused by visceral obesity, may result in downregulated insulin receptor signaling in muscle and further account for glucose intolerance. Increased pancreatic β-cell mass might compensate for the downregulated insulin gene (ins2). Increased glucagon and α-cell mass, accompanied by upregulated glucagon gene (gcg), might also be risk factors for the development of diabetes. Maternal supplementation with BC disturbs lipid metabolism and induces glucose intolerance in F1 female mice, suggesting that BC supplementation during pregnancy shoul...Continue Reading

References

Sep 1, 1992·Annals of Epidemiology·K T Khaw, E Barrett-Connor
Jan 1, 1988·Nutrition and Cancer·A Bendich
Feb 1, 1993·Endocrine Reviews·C BouchardP Mauriège
Aug 15, 1998·Biochemical and Biophysical Research Communications·D L CrandallJ G Kral
May 20, 1999·Annual Review of Pharmacology and Toxicology·M D Collins, G E Mao
Jan 11, 2000·Critical Reviews in Toxicology·R A WoutersenV J Feron
Aug 2, 2001·Nature Medicine·A H BergP E Scherer
Sep 11, 2002·The Journal of Nutrition·Alfred SommerUNKNOWN Annecy Accords
Sep 11, 2002·The Journal of Nutrition·Melissa MillerJoanne Katz
Nov 9, 2002·Bioinformatics·Long-Cheng Li, Rajvir Dahiya
Aug 29, 2003·Cellular and Molecular Life Sciences : CMLS·M L BonetA Palou
Jul 31, 2004·The Journal of Nutrition·Kimberly A MatthewsBruce S Chertow
Apr 20, 2005·Lancet·Robert H EckelPaul Z Zimmet
Jun 29, 2005·Diabetes·Catherine Gallou-Kabani, Claudine Junien
Jul 27, 2006·Genesis : the Journal of Genetics and Development·Robert A WaterlandKajal G Tahiliani
Dec 21, 2007·Diabetes & Metabolism·B Antuna-PuenteJ-P Bastard
Jan 21, 2009·International Journal of Obesity : Journal of the International Association for the Study of Obesity·I M Y SzetoG H Anderson
Feb 20, 2009·International Journal of Andrology·Henry VölzkeHenri Wallaschofski
Jun 15, 2011·Biochimica Et Biophysica Acta·M Luisa BonetAndreu Palou
Jun 16, 2011·PloS One·Jaume AmengualJohannes von Lintig
Jan 13, 2012·Biochemistry and Cell Biology = Biochimie Et Biologie Cellulaire·Antònia Nadal-CasellasMagdalena Gianotti
Jul 7, 2012·Paediatric and Perinatal Epidemiology·Andrew L Thorne-Lyman, Wafaie W Fawzi
Jun 25, 2013·Trends in Endocrinology and Metabolism : TEM·Daniella E Duque-Guimarães, Susan E Ozanne
Nov 27, 2014·Nature Communications·Elmar W TobiBastiaan T Heijmans
Apr 9, 2015·Nature Reviews. Endocrinology·Jonathan E Campbell, Daniel J Drucker
Nov 28, 2015·Molecular Nutrition & Food Research·R Rühl, J F Landrier
Apr 27, 2016·Diabetologia·Young H LeeRoger H Unger
May 9, 2016·The Journal of Nutritional Biochemistry·Estanislau NavarroHelmut Schröder
May 10, 2016·Endocrine Reviews·Alexandra Kautzky-WillerGiovanni Pacini

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Citations

Mar 3, 2020·Biochimica Et Biophysica Acta. Molecular and Cell Biology of Lipids·M Luisa BonetAndreu Palou
Oct 2, 2020·Current Developments in Nutrition·Bryan M GannonSaurabh Mehta

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