The Effects of Maternal Under-Nutrition and a Post-Natal High Fat Diet on Lens Growth, Transparency and Oxidative Defense Systems in Rat Offspring.
A poor early life nutrition environment is well established to result in a range of cardiometabolic disorders in offspring in later life. These effects can be exacerbated via exposure to an obesogenic dietary environment. To date, the effect of maternal diet and/or a post-natal obesogenic nutritional environment on key characteristics related to lens growth and oxidative stress has not been undertaken. The present study, therefore, examined the characteristics and oxidative status of the lens.



Using a model of moderate maternal under-nutrition, rat dams were fed either a control diet (100% ad libitum, CON) or undernourished throughout pregnancy (50% of ad libitum intake, UN) and offspring fed either a control (5% fat, C) or high fat (30% fat, HF) diet post-weaning, resulting in four nutritional groups; CON-C, CON-HF, UN-C, and UN-HF. Offspring lenses were extracted at 160 days of age, weighed, imaged under dark and bright field microscopy, and then dissected into cortical and core fractions for biochemical analyses of oxidative stress markers.



Our findings reveal that lenses from all groups were transparent. However, gender specific changes were evident at the biochemical level with increased oxidative stress detected in the cortex and core of female but not male UN-C lenses, and in the cortex of male but not female CON-HF lenses. The greatest increase in oxidative stress was detected in the UN-HF group in the cortex and core regions of the lens and for both genders.



These findings show that oxidative stress is exacerbated in the lens as a result of a combination of altered pre-natal and post-natal diet. This demonstrates a novel interaction between the two developmental windows and warrants further investigations toward devising appropriate nutritional strategies for minimizing oxidative stress in the lens.
a Department of Physiology, Faculty of Medical and Health Sciences , University of Auckland , Auckland , New Zealand.|b NZ National Eye Centre , University of Auckland , Auckland , New Zealand.|c School of Medical Sciences , University of Auckland , Auckland , New Zealand.
Sachini K
SK
Jayaratne
a Department of Physiology, Faculty of Medical and Health Sciences , University of Auckland , Auckland , New Zealand.|b NZ National Eye Centre , University of Auckland , Auckland , New Zealand.|c School of Medical Sciences , University of Auckland , Auckland , New Zealand.
Paul J
PJ
Donaldson
d Liggins Institute , University of Auckland , Auckland , New Zealand.
Mark H
MH
Vickers
a Department of Physiology, Faculty of Medical and Health Sciences , University of Auckland , Auckland , New Zealand.|b NZ National Eye Centre , University of Auckland , Auckland , New Zealand.|c School of Medical Sciences , University of Auckland , Auckland , New Zealand.
Julie C
JC
Lim
D050154:Adiposity; D000818:Animals; D001205:Ascorbic Acid / Q000378:metabolism; D015415:Biomarkers / Q000378:metabolism; D001786:Blood Glucose / Q000378:metabolism; D001835:Body Weight; D059305:Diet, High-Fat / Q000009:adverse effects*; D005260:Female; D005978:Glutathione / Q000378:metabolism; D007328:Insulin / Q000097:blood; D007905:Lens Diseases / Q000209:etiology* / Q000378:metabolism; D007908:Lens, Crystalline / Q000254:growth & development* / Q000378:metabolism; D020738:Leptin / Q000097:blood; D008297:Male; D044342:Malnutrition / Q000150:complications*; D039382:Maternal Nutritional Physiological Phenomena; D009765:Obesity / Q000209:etiology / Q000378:metabolism; D018384:Oxidative Stress / Q000502:physiology*; D011247:Pregnancy; D051381:Rats; D017207:Rats, Sprague-Dawley; D014810:Vitamin E / Q000378:metabolism
D015415:Biomarkers; D001786:Blood Glucose; D007328:Insulin; D020738:Leptin; D014810:Vitamin E; D005978:Glutathione; D001205:Ascorbic Acid
Cataract; oxidative stress; post-natal nutrition; pre-natal nutrition