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Differential effects of high-energy diets on sensitivity to dopamine receptor antagonists in reducing intake of sucrose and fructose in rats
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Abstracts / Appetite 54 (2010) 631–683
Amylin induces ERK 1/2 phosphorylation in structures of the AP/NTS-LPB-Ce-BSTL axis C.S. POTES ∗ , T. RIEDIGER, T.A. LUTZ Institute of Veterinary Physiology, Zurich Center for Integrative Human Physiology, Zurich University, Zurich, Switzerland
CD36 receptor expression on the tongue is differentially affected by high fat diet in obesity-prone and obesity-resistant rats S.D. PRIMEAUX ∗ , H.D. BRAYMER, G.A. BRAY Pennington Biomedical Research Center, Baton Rouge, LA, USA
Peripheral amylin inhibits food intake via activation of the area postrema (AP). The extracellular-signal regulated kinase 1 and 2 (ERK) cascade mediates cholecystokinin anorexia via the nucleus of the solitary tract (NTS). Amylin induces ERK phosphorylation (pERK) in osteoclasts, so it might also activate this cascade in AP neurons. Further, previous studies had shown that a high number of amylin activated neurons in the AP are noradrenergic as they express dopamine-beta-hydroxylase (DBH). Hence, we investigated in immunohistochemical experiments whether amylin activates the ERK cascade in the AP and downstream, in synaptically activated areas. Furthermore, we phenotyped the pERK-positive AP-neurons using DBH as a marker for noradrenergic neurons. To evaluate the time-course of amylin-induced pERK, we injected 24 h fasted rats with saline or amylin (5 or 20 g/kg, SC) and perfused the animals 10, 15, 20 or 30 min later. Brain sections containing the AP, NTS, lateral parabrachial nucleus (LPB), central nucleus of amygdala (Ce) and lateral bed nucleus of stria terminalis (BSTL) were stained for pERK. The peak of ERK phosphorylation in the AP occurred between 10 and 15 min after amylin treatment; 22% of pERK-positive neurons in the AP were noradrenergic. The other analyzed areas also showed amylin-induced pERK. These results show that amylin stimulates pERK in the AP-BSTL axis and that a subpopulation of amylin-responsive AP neurons are noradrenergic. These findings suggest a potential role of pERK signaling in amylin’s anorectic effect. doi:10.1016/j.appet.2010.04.164
There are individuals that are susceptible to becoming obese when consuming a high-fat diet (HFD), while others are resistant to becoming obese when consuming a HFD. The detection of dietary fat in the mouth plays an important role in the consumption of dietary fat. Therefore, individual differences in the detection of dietary fat by the mouth are probable. The current experiment was conducted to determine differences in the expression of the fatty acid receptor, CD36, on the tongues of obesity-prone (OsborneMendel; OM) and obesity-resistant (S5B) rats fed a HFD. OM and S5B rats were fed either a standard chow diet, a HFD or a low fat diet (LFD) for 1 day, 3 days or 14 days. CD36 receptor mRNA expression was measured by real-time PCR from the circumvallate papillae of the tongue, which has been shown to have the highest concentration of CD36 receptor mRNA on the tongue. CD36 receptor mRNA levels did not differ between OM and S5B rats fed a chow diet. In S5B rats, CD36 receptor mRNA levels on the circumvallate papillae were increased within 1d of access to the HFD, however, this effect was transient and was diminished by 3d. Unlike S5B rats, OM rats did not exhibit an initial increase in CD36 receptor mRNA levels on the circumvallate papillae following 1d access to the HFD. The consumption of a HFD increased CD36 receptor mRNA levels on the circumvallate papillae of OM rats at 3d and 14d. These data suggest that HFD affects CD36 receptor mRNA expression in a time and strain dependent manner and may play a role in the detection of HFD by the mouth. doi:10.1016/j.appet.2010.04.166
Centrally administered QRFP-26 increases high fat intake in female rats S.D. PRIMEAUX ∗ , H.D. BRAYMER, G.A. BRAY Pennington Biomedical Research Center, Baton Rouge, LA, USA QRFP is strongly conserved across vertebrates and is a member of the RFamide-related peptides, with the motif Arg-Phe-NH2 at the C-terminal end. In rodents, QRFP is expressed in localized regions of the mediobasal hypothalamus which are abundant in neurotransmitters, neuropeptides and receptors systems that are important for food intake regulation and reproductive behaviors. Our previous experiments have reported an increase in the intake of a high fat diet (HFD), but not a low fat diet (LFD) in male rats following central administration of QRFP-26. The current experiments were conducted to investigate the effects of centrally administered QRFP-26 on the intake of a HFD (60% kcal from fat) in female rats and to determine if hypothalamic QRFP mRNA levels were affected by estrous cycle. In Experiment 1, randomly cycling female rats were administered varying doses of QRFP-26 (0.3 nM, 0.5 nM, 1.0 nM) via lateral ventricle cannula. All doses of QRFP-26 administered increased the intake of the HFD, but not LFD (10% kcal from fat) in female rats. In Experiment 2, estrous cycle was monitored daily and brains were removed during diestrous, proestrous, or estrous. Real-time PCR was used to determine the levels of prepro-QRFP mRNA in specific regions of the hypothalamus (paraventricular nucleus, lateral hypothalamus, and ventromedial/arcuate nucleus (VMH/ARC)). The level of prepro-QRFP mRNA in the VMH/ARC was affected by estrous cycle, and was increased during proestrous. These data suggest that QRFP-26 plays a role in both feeding behavior, specifically high fat feeding, and reproductive status in female rats. doi:10.1016/j.appet.2010.04.165
Differential effects of high-energy diets on sensitivity to dopamine receptor antagonists in reducing intake of sucrose and fructose in rats C.E. PRITCHETT 1,∗ , A. CONTEH 2 , A. HAJNAL 1 1 Dept. of Neural & Behavioral Sciences, Penn State Univ., Coll. Med., Hershey, PA, USA 2 Purdue Univ., West Lafayette, IN, USA To investigate how high energy diets influence the reward system’s responsiveness to palatable carbohydrates (CHOs), Sprague–Dawley male rats were fed high fat low CHO (60 and 20%kcal, 4.1 kcal/g, VHF; n = 11) or moderate fat high CHO (32 and 51%kcal, 4.6 kcal/g, HFHC; n = 11) or chow (3.3 kcal/g, n = 8) for 24 weeks. 2-h one-bottle intake of isocaloric 0.3 M sucrose and 0.4 M fructose was tested following i.p. administration of equimolar doses (0, 50, 200, 400, 600 nmol/kg) of dopamine D1 (SCH23390; SCH) or D2 (Raclopride; RAC) receptor antagonists. Whereas both antagonists reduced CHO intake dose-dependently, the effects varied with respect to the diets and test solutions. SCH suppressed intake of sucrose equally in all diet groups. For fructose, SCH only reduced intake at higher concentrations, with VHF rats being more sensitive (40% vs. 20–25% reduction at 200 nmol/kg, p > 0.001). Except at the highest dose, RAC produced significant effects for sucrose only in VHF rats (200 nmol/kg: 61%, p > 0.01; 400 nmol/kg: 57%, p > 0.01). In contrast, for fructose the HFHC rats showed the largest suppression of intake to RAC (200 nmol/kg: 49%, p > 0.01; 400 nmol: 45%, p > 0.001; 600 nmol: 44%, p > 0.001), while VHF rats were insensitive to all but 600 nmol/kg. These findings show that dietary fat and CHOs coupled with chronic high energy intake may alter dopamine signaling, and that ingestion of fructose and sucrose may recruit different mechanisms of reward. doi:10.1016/j.appet.2010.04.167
Abstracts / Appetite 54 (2010) 631–683
Amylin induces ERK 1/2 phosphorylation in structures of the AP/NTS-LPB-Ce-BSTL axis C.S. POTES ∗ , T. RIEDIGER, T.A. LUTZ Institute of Veterinary Physiology, Zurich Center for Integrative Human Physiology, Zurich University, Zurich, Switzerland
CD36 receptor expression on the tongue is differentially affected by high fat diet in obesity-prone and obesity-resistant rats S.D. PRIMEAUX ∗ , H.D. BRAYMER, G.A. BRAY Pennington Biomedical Research Center, Baton Rouge, LA, USA
Peripheral amylin inhibits food intake via activation of the area postrema (AP). The extracellular-signal regulated kinase 1 and 2 (ERK) cascade mediates cholecystokinin anorexia via the nucleus of the solitary tract (NTS). Amylin induces ERK phosphorylation (pERK) in osteoclasts, so it might also activate this cascade in AP neurons. Further, previous studies had shown that a high number of amylin activated neurons in the AP are noradrenergic as they express dopamine-beta-hydroxylase (DBH). Hence, we investigated in immunohistochemical experiments whether amylin activates the ERK cascade in the AP and downstream, in synaptically activated areas. Furthermore, we phenotyped the pERK-positive AP-neurons using DBH as a marker for noradrenergic neurons. To evaluate the time-course of amylin-induced pERK, we injected 24 h fasted rats with saline or amylin (5 or 20 g/kg, SC) and perfused the animals 10, 15, 20 or 30 min later. Brain sections containing the AP, NTS, lateral parabrachial nucleus (LPB), central nucleus of amygdala (Ce) and lateral bed nucleus of stria terminalis (BSTL) were stained for pERK. The peak of ERK phosphorylation in the AP occurred between 10 and 15 min after amylin treatment; 22% of pERK-positive neurons in the AP were noradrenergic. The other analyzed areas also showed amylin-induced pERK. These results show that amylin stimulates pERK in the AP-BSTL axis and that a subpopulation of amylin-responsive AP neurons are noradrenergic. These findings suggest a potential role of pERK signaling in amylin’s anorectic effect. doi:10.1016/j.appet.2010.04.164
There are individuals that are susceptible to becoming obese when consuming a high-fat diet (HFD), while others are resistant to becoming obese when consuming a HFD. The detection of dietary fat in the mouth plays an important role in the consumption of dietary fat. Therefore, individual differences in the detection of dietary fat by the mouth are probable. The current experiment was conducted to determine differences in the expression of the fatty acid receptor, CD36, on the tongues of obesity-prone (OsborneMendel; OM) and obesity-resistant (S5B) rats fed a HFD. OM and S5B rats were fed either a standard chow diet, a HFD or a low fat diet (LFD) for 1 day, 3 days or 14 days. CD36 receptor mRNA expression was measured by real-time PCR from the circumvallate papillae of the tongue, which has been shown to have the highest concentration of CD36 receptor mRNA on the tongue. CD36 receptor mRNA levels did not differ between OM and S5B rats fed a chow diet. In S5B rats, CD36 receptor mRNA levels on the circumvallate papillae were increased within 1d of access to the HFD, however, this effect was transient and was diminished by 3d. Unlike S5B rats, OM rats did not exhibit an initial increase in CD36 receptor mRNA levels on the circumvallate papillae following 1d access to the HFD. The consumption of a HFD increased CD36 receptor mRNA levels on the circumvallate papillae of OM rats at 3d and 14d. These data suggest that HFD affects CD36 receptor mRNA expression in a time and strain dependent manner and may play a role in the detection of HFD by the mouth. doi:10.1016/j.appet.2010.04.166
Centrally administered QRFP-26 increases high fat intake in female rats S.D. PRIMEAUX ∗ , H.D. BRAYMER, G.A. BRAY Pennington Biomedical Research Center, Baton Rouge, LA, USA QRFP is strongly conserved across vertebrates and is a member of the RFamide-related peptides, with the motif Arg-Phe-NH2 at the C-terminal end. In rodents, QRFP is expressed in localized regions of the mediobasal hypothalamus which are abundant in neurotransmitters, neuropeptides and receptors systems that are important for food intake regulation and reproductive behaviors. Our previous experiments have reported an increase in the intake of a high fat diet (HFD), but not a low fat diet (LFD) in male rats following central administration of QRFP-26. The current experiments were conducted to investigate the effects of centrally administered QRFP-26 on the intake of a HFD (60% kcal from fat) in female rats and to determine if hypothalamic QRFP mRNA levels were affected by estrous cycle. In Experiment 1, randomly cycling female rats were administered varying doses of QRFP-26 (0.3 nM, 0.5 nM, 1.0 nM) via lateral ventricle cannula. All doses of QRFP-26 administered increased the intake of the HFD, but not LFD (10% kcal from fat) in female rats. In Experiment 2, estrous cycle was monitored daily and brains were removed during diestrous, proestrous, or estrous. Real-time PCR was used to determine the levels of prepro-QRFP mRNA in specific regions of the hypothalamus (paraventricular nucleus, lateral hypothalamus, and ventromedial/arcuate nucleus (VMH/ARC)). The level of prepro-QRFP mRNA in the VMH/ARC was affected by estrous cycle, and was increased during proestrous. These data suggest that QRFP-26 plays a role in both feeding behavior, specifically high fat feeding, and reproductive status in female rats. doi:10.1016/j.appet.2010.04.165
Differential effects of high-energy diets on sensitivity to dopamine receptor antagonists in reducing intake of sucrose and fructose in rats C.E. PRITCHETT 1,∗ , A. CONTEH 2 , A. HAJNAL 1 1 Dept. of Neural & Behavioral Sciences, Penn State Univ., Coll. Med., Hershey, PA, USA 2 Purdue Univ., West Lafayette, IN, USA To investigate how high energy diets influence the reward system’s responsiveness to palatable carbohydrates (CHOs), Sprague–Dawley male rats were fed high fat low CHO (60 and 20%kcal, 4.1 kcal/g, VHF; n = 11) or moderate fat high CHO (32 and 51%kcal, 4.6 kcal/g, HFHC; n = 11) or chow (3.3 kcal/g, n = 8) for 24 weeks. 2-h one-bottle intake of isocaloric 0.3 M sucrose and 0.4 M fructose was tested following i.p. administration of equimolar doses (0, 50, 200, 400, 600 nmol/kg) of dopamine D1 (SCH23390; SCH) or D2 (Raclopride; RAC) receptor antagonists. Whereas both antagonists reduced CHO intake dose-dependently, the effects varied with respect to the diets and test solutions. SCH suppressed intake of sucrose equally in all diet groups. For fructose, SCH only reduced intake at higher concentrations, with VHF rats being more sensitive (40% vs. 20–25% reduction at 200 nmol/kg, p > 0.001). Except at the highest dose, RAC produced significant effects for sucrose only in VHF rats (200 nmol/kg: 61%, p > 0.01; 400 nmol/kg: 57%, p > 0.01). In contrast, for fructose the HFHC rats showed the largest suppression of intake to RAC (200 nmol/kg: 49%, p > 0.01; 400 nmol: 45%, p > 0.001; 600 nmol: 44%, p > 0.001), while VHF rats were insensitive to all but 600 nmol/kg. These findings show that dietary fat and CHOs coupled with chronic high energy intake may alter dopamine signaling, and that ingestion of fructose and sucrose may recruit different mechanisms of reward. doi:10.1016/j.appet.2010.04.167