Voluntary post weaning exercise restores metabolic homeostasis in offspring of obese rats.
OBJECTIVE
Physical exercise reduces obesity, insulin resistance and dyslipidemia. We previously found that maternal obesity alters central appetite circuits and contributes to increased adiposity, glucose intolerance and metabolic disease in offspring. Here we hypothesized that voluntary exercise would ameliorate the adverse metabolic effects of maternal obesity on offspring.


RESULTS
Sprague-Dawley females fed chow (C) or high-fat diet HFD (H) were mated. Female offspring from C dams were weaned onto chow (CC); those from H dams recieved chow (HC) or HFD (HH). Half of each group was provided with running wheels (CC(EX), HC(EX), HH(EX); n=10-12). Maternal obesity increased body weight (12%), adiposity, plasma lipids and induced glucose intolerance (HC vs CC; P<0.05). These were exaggerated by postweaning HFD (HH vs HC; P<0.01), showed doubled energy intake, a 37% increase in body weight, insulin resistance and glucose intolerance (HH vs HC; P<0.01). Exercise reduced fat mass, plasma lipids, HOMA and fasting glucose in HC(EX) (vs HC; P<0.05) and HH(EX) (vs HH; P<0.01). Values in HC(EX) were indistinguishable from CC, however in HH(EX) these metabolic parameters remained higher than the sedentary HC and CC rats (P<0.01). mRNA expression of hypothalamic pro-opiomelanocortin, and adipose tumour necrosis factor α and 11β-hydroxysteroid dehydrogenase type 1 were reduced by exercise in HH(EX) (vs HH; P<0.05).


CONCLUSIONS
While voluntary exercise almost completely reversed the metabolic effects of maternal obesity in chow fed offspring, it did not fully attenuate the increased adiposity, glucose intolerance and insulin resistance in offspring weaned onto HFD.
School of Medical Sciences, University of New South Wales, Sydney, NSW 2052, Australia.
S
S
Rajia
H
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Chen
M J
MJ
Morris
D043205:11-beta-Hydroxysteroid Dehydrogenase Type 1 / Q000097:blood; D050154:Adiposity; D000824:Animal Nutritional Physiological Phenomena; D000818:Animals; D001066:Appetite / Q000502:physiology; D001786:Blood Glucose / Q000032:analysis; D001794:Blood Pressure; D001835:Body Weight; D059305:Diet, High-Fat; D050171:Dyslipidemias / Q000378:metabolism; D002149:Energy Intake; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005260:Female; D006706:Homeostasis / Q000502:physiology*; D007031:Hypothalamus / Q000378:metabolism; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D020738:Leptin / Q000097:blood; D039382:Maternal Nutritional Physiological Phenomena; D009765:Obesity / Q000378:metabolism*; D010805:Physical Conditioning, Animal / Q000502:physiology*; D011333:Pro-Opiomelanocortin / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D014280:Triglycerides / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D014886:Weaning
D001786:Blood Glucose; D005230:Fatty Acids, Nonesterified; D007328:Insulin; D020738:Leptin; D012333:RNA, Messenger; D014280:Triglycerides; D014409:Tumor Necrosis Factor-alpha; D011333:Pro-Opiomelanocortin; D043205:11-beta-Hydroxysteroid Dehydrogenase Type 1