In utero Exposure to Germinated Brown Rice and Its GABA Extract Attenuates High-Fat-Diet-Induced Insulin Resistance in Rat Offspring

2017 ◽  
Vol 10 (1-2) ◽  
pp. 19-31 ◽  
Author(s):  
Hadiza Altine Adamu ◽  
Mustapha Umar Imam ◽  
Ooi Der-Jiun ◽  
Maznah Ismail
PLoS ONE ◽  
2014 ◽  
Vol 9 (1) ◽  
pp. e84209 ◽  
Author(s):  
Sarah J. Borengasser ◽  
Ping Kang ◽  
Jennifer Faske ◽  
Horacio Gomez-Acevedo ◽  
Michael L. Blackburn ◽  
...  

2014 ◽  
Vol 210 (1) ◽  
pp. S42-S43
Author(s):  
Melissa Suter ◽  
Jun Ma ◽  
Patricia Vuguin ◽  
Kirsten Hartil ◽  
Ariana Fiallo ◽  
...  

2014 ◽  
Vol 46 (23) ◽  
pp. 841-850 ◽  
Author(s):  
Sarah J. Borengasser ◽  
Jennifer Faske ◽  
Ping Kang ◽  
Michael L. Blackburn ◽  
Thomas M. Badger ◽  
...  

The proportion of pregnant women who are obese at conception continues to rise. Compelling evidence suggests the intrauterine environment is an important determinant of offspring health. Maternal obesity and unhealthy diets are shown to promote metabolic programming in the offspring. Mitochondria are maternally inherited, and we have previously shown impaired mitochondrial function in rat offspring exposed to maternal obesity in utero. Mitochondrial health is maintained by mitochondrial dynamics, or the processes of fusion and fission, which serve to repair damaged mitochondria, remove irreparable mitochondria, and maintain mitochondrial morphology. An imbalance between fusion and fission has been associated with obesity, insulin resistance, and reproduction complications. In the present study, we examined the influence of maternal obesity and postweaning high-fat diet (HFD) on key regulators of mitochondrial fusion and fission in rat offspring at important developmental milestones which included postnatal day (PND)35 (2 wk HFD) and PND130 (∼16 wk HFD). Our results indicate HFD-fed offspring had reduced mRNA expression of presenilin-associated rhomboid-like (PARL), optic atrophy (OPA)1, mitofusin (Mfn)1, Mfn2, fission (Fis)1, and nuclear respiratory factor (Nrf)1 at PND35, while OPA1 and Mfn2 remained decreased at PND130. Putative transcriptional regulators of mitochondrial dynamics were reduced in rat placenta and offspring liver and skeletal muscle [peroxisome proliferator-activated receptor gamma coactivator (PGC1)α, PGC1β, and estrogen-related receptor (ERR)α], consistent with indirect calorimetry findings revealing reduced energy expenditure and impaired fat utilization. Overall, maternal obesity detrimentally alters mitochondrial targets that may contribute to impaired mitochondrial health and increased obesity susceptibility in later life.


2017 ◽  
Vol 81 (5) ◽  
pp. 979-986 ◽  
Author(s):  
Hsueh-Wei Yen ◽  
Hui-Li Lin ◽  
Chi-Long Hao ◽  
Fu-Chih Chen ◽  
Chun-Yun Chen ◽  
...  

Endocrinology ◽  
2003 ◽  
Vol 144 (2) ◽  
pp. 500-508 ◽  
Author(s):  
Li Chen ◽  
B. L. G. Nyomba

High-fat diet and intrauterine growth retardation may predispose to obesity, insulin resistance, and type 2 diabetes. Because prenatal ethanol (ETOH) exposure causes intrauterine growth retardation, we investigated its interactions with postnatal high-fat diet on glucose tolerance and adipocyte-derived hormones in the rat offspring. High-fat-fed offspring had increased adiposity, serum leptin, and muscle uncoupling protein-3, but decreased adiponectin mRNA, compared with corresponding chow-fed groups. ETOH-exposed offspring had normal adiponectin, but increased resistin mRNA and protein, compared with controls, regardless of postnatal diet. Skeletal muscle glucose transporter-4 content was decreased after both ETOH exposure and high-fat feeding. Glycemic and insulin responses to an ip glucose challenge were equally increased in non-ETOH-exposed high-fat-fed offspring and in ETOH-exposed chow-fed offspring, with additive effects of ETOH and high-fat diet. Pancreatic insulin content was elevated only in non-ETOH-exposed high-fat-fed offspring. The data suggest that high-fat diet worsens glucose intolerance in offspring of rats exposed to ETOH. Prenatal ETOH exposure and postnatal high-fat diet might cause insulin resistance through separate mechanisms, involving resistin and adiponectin, respectively.


2016 ◽  
Vol 59 (1) ◽  
pp. 39-44 ◽  
Author(s):  
Kuo-Ping Shen ◽  
Chi-Long Hao ◽  
Hsueh-Wei Yen ◽  
Chun-Yen Chen ◽  
Jia-Hao Chen ◽  
...  

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