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Alterations in sucrose sham-feeding intake as a function of diet-exposure in rats maintained on calorically dense diets.

ABSTRACT: We previously reported that rats increase meal size upon initial presentation of a calorically dense diet. The increase may be attributed to increased orosensory stimulation and/or reduced sensitivity to post-ingestive inhibitory signals. During feeding both types of signals are simultaneously in play; thus here, we compare responses in rats presented a high-energy diet (HE) or 45% high-fat diet (HF) with those of chow-fed controls (CHOW) in a sham-feeding procedure in which post-ingestive feedback is minimized. Measures of sham-feeding to sucrose were taken before diet manipulation (baseline), ~5 days (dynamic phase) and ~6 weeks (static phase) following introduction of the palatable diet, as well as after animals were switched back to standard chow (recovery phase). Some but not all the hypotheses based on our previous findings were confirmed by the outcomes here. Consistent with our hypothesis that enhanced orosensory stimulation during the dynamic phase compared with the static phase would generalize to increased intake of other palatable stimuli, HE rats showed higher sucrose intake during the dynamic phase compared with the static phase. Contrary to what we hypothesized, HE and HF rats did not increase responses to sucrose compared to CHOW rats. In fact, HE rats showed decreased responses compared to CHOW controls. Thus changes in orosensory stimulation do not necessarily generalize to increased intake of other palatable stimuli.

SUBMITTER: Treesukosol Y

PROVIDER: S-EPMC4499488 | biostudies-literature | 2015 Sep

REPOSITORIES: biostudies-literature

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Alterations in sucrose sham-feeding intake as a function of diet-exposure in rats maintained on calorically dense diets.

Treesukosol Yada Y Liang Nu-Chu NC Moran Timothy H TH

Appetite 20150515

We previously reported that rats increase meal size upon initial presentation of a calorically dense diet. The increase may be attributed to increased orosensory stimulation and/or reduced sensitivity to post-ingestive inhibitory signals. During feeding both types of signals are simultaneously in play; thus here, we compare responses in rats presented a high-energy diet (HE) or 45% high-fat diet (HF) with those of chow-fed controls (CHOW) in a sham-feeding procedure in which post-ingestive feedb ...[more]

PMID: 25987540

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Project description:BACKGROUND:Malignant brain cancer persists as a major disease of morbidity and mortality in adults and is the second leading cause of cancer death in children. Many current therapies for malignant brain tumors fail to provide long-term management because they ineffectively target tumor cells while negatively impacting the health and vitality of normal brain cells. In contrast to brain tumor cells, which lack metabolic flexibility and are largely dependent on glucose for growth and survival, normal brain cells can metabolize both glucose and ketone bodies for energy. This study evaluated the efficacy of KetoCal, a new nutritionally balanced high fat/low carbohydrate ketogenic diet for children with epilepsy, on the growth and vascularity of a malignant mouse astrocytoma (CT-2A) and a human malignant glioma (U87-MG). METHODS:Adult mice were implanted orthotopically with the malignant brain tumors and KetoCal was administered to the mice in either unrestricted amounts or in restricted amounts to reduce total caloric intake according to the manufacturers recommendation for children with refractory epilepsy. The effects KetoCal on tumor growth, vascularity, and mouse survival were compared with that of an unrestricted high carbohydrate standard diet. RESULTS:KetoCal administered in restricted amounts significantly decreased the intracerebral growth of the CT-2A and U87-MG tumors by about 65% and 35%, respectively, and significantly enhanced health and survival relative to that of the control groups receiving the standard low fat/high carbohydrate diet. The restricted KetoCal diet reduced plasma glucose levels while elevating plasma ketone body (beta-hydroxybutyrate) levels. Tumor microvessel density was less in the calorically restricted KetoCal groups than in the calorically unrestricted control groups. Moreover, gene expression for the mitochondrial enzymes, beta-hydroxybutyrate dehydrogenase and succinyl-CoA: 3-ketoacid CoA transferase, was lower in the tumors than in the contralateral normal brain suggesting that these brain tumors have reduced ability to metabolize ketone bodies for energy. CONCLUSION:The results indicate that KetoCal has anti-tumor and anti-angiogenic effects in experimental mouse and human brain tumors when administered in restricted amounts. The therapeutic effect of KetoCal for brain cancer management was due largely to the reduction of total caloric content, which reduces circulating glucose required for rapid tumor growth. A dependency on glucose for energy together with defects in ketone body metabolism largely account for why the brain tumors grow minimally on either a ketogenic-restricted diet or on a standard-restricted diet. Genes for ketone body metabolism should be useful for screening brain tumors that could be targeted with calorically restricted high fat/low carbohydrate ketogenic diets. This preclinical study indicates that restricted KetoCal is a safe and effective diet therapy and should be considered as an alternative therapeutic option for malignant brain cancer.

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Dataset Information

Alterations in sucrose sham-feeding intake as a function of diet-exposure in rats maintained on calorically dense diets.

Publications

Alterations in sucrose sham-feeding intake as a function of diet-exposure in rats maintained on calorically dense diets.

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