Rats eat a cafeteria-style diet to excess but eat smaller amounts and less frequently when tested with chow.

Background: Obesity is associated with excessive consumption of palatable, energy dense foods. The present study used an animal model to examine feeding patterns during exposure to and withdrawal from these foods.

Methods: Male Sprague Dawley rats were exposed to standard lab chow only (Chow rats) or a range of cafeteria-style foods eaten by people (Caf rats).

Extended exposure to a palatable cafeteria diet alters gene expression in brain regions implicated in reward, and withdrawal from this diet alters gene expression in brain regions associated with stress.

Like people, rodents exposed to energy-rich foods over-eat and become overweight. Removal of this diet activates stress systems, which may explain why people have difficulty dieting. We exposed rats to energy-rich foods in order to identify changes in the brain induced by that diet and by its removal.

Experimental hyperleptinemia in neonatal rats leads to selective leptin responsiveness, hypertension, and altered myocardial function.

The prevalence of obesity among pregnant women is increasing. Evidence from human cohort studies and experimental animals suggests that offspring cardiovascular and metabolic function is compromised through early life exposure to maternal obesity. Previously, we reported that juvenile offspring of obese rats develop sympathetically mediated hypertension associated with neonatal hyperleptinemia.

Metabolic parameters and emotionality are little affected in G-protein coupled receptor 12 (Gpr12) mutant mice.

Background: G-protein coupled receptors (GPR) bear the potential to serve as yet unidentified drug targets for psychiatric and metabolic disorders. GPR12 is of major interest given its putative role in metabolic function and its unique brain distribution, which suggests a role in emotionality and affect. We tested Gpr12 deficient mice in a series of metabolic and behavioural tests and subjected them to a well-established high-fat diet feeding protocol.

Neurological and stress related effects of shifting obese rats from a palatable diet to chow and lean rats from chow to a palatable diet.

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.

High-fat diet decreases tyrosine hydroxylase mRNA expression irrespective of obesity susceptibility in mice.

Tyrosine hydroxylase is the rate-limiting enzyme in the synthesis of dopamine, a key neurotransmitter in the regulation of food intake. This study examined tyrosine hydroxylase mRNA expression in obese mice fed a high-fat diet. After 8 week feeding of high-fat diet mice were classified as diet-induced obese and obese-resistant according to body weight gain.

High-fat diet exposure increases dopamine D2 receptor and decreases dopamine transporter receptor binding density in the nucleus accumbens and caudate putamen of mice.

This experiment examined dopamine D2 receptor and its transporter (DAT) density in mice fed a high-fat or low-fat diet for twenty days as well as fed twenty days of high-fat diet then changed to low-fat diet for one and seven days. Quantitative autoradiography revealed that twenty days of high-fat diet consumption significantly increased D2 receptor and decreased DAT density in the dorsal and ventral parts of the caudal caudate putamen (D2: 32% and 35% respectively, DAT: 33.3% and 28.

AM 251 and beta-Funaltrexamine reduce fat intake in a fat-preferring strain of mouse.

This experiment aimed to examine the role of the CB1 and Opioid mu receptors on fat preference by administering the CB1 inverse agonist AM 251 (5mg/kg i.p.) and the opioid mu antagonist beta-Funaltrexamine (15mg/kg s.