title: Neurological and stress related effects of shifting obese rats from a palatable diet to chow and lean rats from chow to a palatable diet.
abstract: Rats exposed to an energy rich, cafeteria diet overeat and become obese. The present experiment examined the neural and behavioural effects of shifting obese rats from this diet to chow and lean rats from chow to the cafeteria diet. Two groups of male Sprague Dawley rats (n=24) were fed either highly palatable cafeteria diet or regular chow (30% vs. 12% energy as fat) for 16 weeks. Half of each group (n=12) was then switched to the opposing diet while the remainder continued on their original diet. The effects of diet switch on the response to restraint stress were assessed and rats were euthanised nine days after diet reversal. After 16 weeks of cafeteria diet, rats were 27% heavier than controls. Rats switched from chow to cafeteria diet (Ch-Caf) became hyperphagic and had increased dopamine D1, D2 and tyrosine hydroxylase mRNA expression in the ventral tegmental area (VTA) compared to rats switched from cafeteria to chow (Caf-Ch). Caf-Ch rats were hypophagic with significant reductions in white (16%) and brown (32%) adipose tissue mass, plasma leptin (34%) and fasting glucose (22%) compared to rats remaining on the cafeteria diet (Caf-Caf). Caf-Caf rats had an elevated plasma corticosterone response to restraint stress compared to Ch-Caf rats indicating that acute but not chronic consumption of palatable cafeteria diet may protect against stress. Caf-Ch rats had increased corticotropin releasing hormone mRNA expression in the dorsal hypothalamus compared to Ch-Ch rats implying that removal of the palatable diet activated the HPA axis. The results were discussed in terms of the links between palatability of diet, obesity and stress.
authors.affiliation: University of New South Wales, NSW 2052, Australia.
authors.forename: Timothy
authors.initials: T
authors.lastname: South
authors.forename: Fred
authors.initials: F
authors.lastname: Westbrook
authors.forename: Margaret J
authors.initials: MJ
authors.lastname: Morris
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism; D000818:Animals; D001786:Blood Glucose / Q000187:drug effects / Q000378:metabolism; D001835:Body Weight; D003345:Corticosterone / Q000097:blood; D003346:Corticotropin-Releasing Hormone / Q000096:biosynthesis; D059305:Diet, High-Fat / Q000009:adverse effects / Q000523:psychology*; D005247:Feeding Behavior / Q000187:drug effects / Q000523:psychology; D007031:Hypothalamus / Q000378:metabolism*; D020738:Leptin / Q000097:blood; D008297:Male; D009765:Obesity / Q000097:blood / Q000139:chemically induced / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D017447:Receptors, Dopamine D1 / Q000096:biosynthesis; D017448:Receptors, Dopamine D2 / Q000096:biosynthesis; D013315:Stress, Psychological / Q000097:blood / Q000378:metabolism* / Q000523:psychology*; D014446:Tyrosine 3-Monooxygenase / Q000096:biosynthesis; D017557:Ventral Tegmental Area / Q000378:metabolism*
chemical_list: D001786:Blood Glucose; D020738:Leptin; D017447:Receptors, Dopamine D1; D017448:Receptors, Dopamine D2; D003346:Corticotropin-Releasing Hormone; D014446:Tyrosine 3-Monooxygenase; D003345:Corticosterone