scholarly journals Midbrain and lateral nucleus accumbens dopamine depletion affects free-choice high-fat high-sugar diet preference in male rats

2020 ◽  
Author(s):  
Anil Joshi ◽  
Fanny Faivre ◽  
Susanne Eva la Fleur ◽  
Michel Barrot
Keyword(s):  
Nucleus Accumbens ◽  
Food Intake ◽  
Free Choice ◽  
Food Preference ◽  
Control Diet ◽  
Dorsal Striatum ◽  
Fat Intake ◽  
Dopamine Depletion ◽  
Medial Nucleus ◽  
Lateral Nucleus

ABSTRACTDopamine influences food intake behavior. Reciprocally, food intake, especially of palatable dietary items, can modulate dopamine-related brain circuitries. Among these reciprocal impacts, it has been observed that an increased intake of dietary fat results in blunted dopamine signaling and, to compensate this lowered dopamine function, caloric intake may subsequently increase. To determine how dopamine regulates food preference we did 6-hydroxydopamine (6-OHDA) lesions, depleting dopamine in specific brain regions in male Sprague Dawley rats. The food preference was assessed by providing the rats with free choice access to control diet, fat, 20% sucrose and tap water. Rats with midbrain lesions targeting the substantia nigra (which is also a model of Parkinson’s disease) consumed fewer calories, as reflected by a decrease in control diet intake, but they surprisingly displayed an increase in fat intake, without change in the sucrose solution intake compared to sham animals. To determine which of the midbrain dopamine projections may contribute to this effect, we next compared the impact of 6-OHDA lesions of terminal fields, targeting the dorsal striatum, the lateral nucleus accumbens and the medial nucleus accumbens. We found that 6-OHDA lesion of the lateral nucleus accumbens, but not of the dorsal striatum or the medial nucleus accumbens, led to increased fat intake. These findings indicate a role for lateral nucleus accumbens dopamine in regulating food preference, in particularly the intake of fat.HIGHLIGHTSDopamine influences fat intakeAnimal model of Parkinson’s disease display lower kcal intake but increased fat choiceDopamine depletion in the lateral nucleus accumbens favors fat intake

scholarly journals μ-Opioid receptor stimulation in the nucleus accumbens elevates fatty tastant intake by increasing palatability and suppressing satiety signals

2011 ◽  
Vol 301 (1) ◽  
pp. R244-R254 ◽  
Author(s):  
Yoshihiro Katsuura ◽  
Jennifer A. Heckmann ◽  
Sharif A. Taha
Keyword(s):  
Nucleus Accumbens ◽  
Food Intake ◽  
Opioid Receptor ◽  
Third Ventricle ◽  
Fat Intake ◽  
High Fat ◽  
Drug Infusion ◽  
Physiological Mechanisms ◽  
Fatty Food ◽  
Μ Opioid Receptor

Infusion of a μ-opioid receptor (MOR) agonist into the nucleus accumbens (NAcc) drives voracious food intake, an effect hypothesized to occur through increased tastant palatability. While intake of many palatable foods is elevated by MOR stimulation, this manipulation has a preferential effect on fatty food ingestion. Consumption of high-fat foods is increased by NAcc MOR stimulation even in rats that prefer a carbohydrate-rich alternative under baseline conditions. This suggests that NAcc MOR stimulation may not simply potentiate palatability signals and raises the possibility that mechanisms mediating fat intake may be distinct from those underlying intake of other tastants. The present study was conducted to investigate the physiological mechanisms underlying the effects of NAcc MOR stimulation on fatty food intake. In experiment 1, we analyzed lick microstructure in rats ingesting Intralipid to identify the changes underlying feeding induced by infusion of a MOR-specific agonist into the NAcc. MOR stimulation in the NAcc core, but not shell, increased burst duration and first-minute licks, while simultaneously increasing the rate and duration of Intralipid ingestion. These results suggest that MOR activation in the core increases Intralipid palatability and attenuates inhibitory postingestive feedback. In experiment 2, we measured the effects of MOR stimulation in the NAcc core on consumption of nonnutritive olestra. A MOR-specific agonist dose dependently increased olestra intake, demonstrating that caloric signaling is not required for hyperphagia induced by NAcc MOR stimulation. Feeding induced by drug infusion in both experiments 1 and 2 was blocked by a MOR antagonist. In experiment 3, we determined whether MOR activation in the NAcc core could attenuate satiety-related signaling caused by infusion of the melanocortin agonist MTII into the third ventricle. Suppression of intake caused by MTII was reversed by MOR stimulation. Together, our results suggest that MOR stimulation in the NAcc core elevates fatty food intake through palatability mechanisms dependent on orosensory cues and suppression of satiety signals inhibiting food intake.

scholarly journals Impaired branched chain amino acid metabolism alters feeding behavior and increases orexigenic neuropeptide expression in the hypothalamus

2011 ◽  
Vol 212 (1) ◽  
pp. 85-94 ◽  
Author(s):  
Megan N Purpera ◽  
Li Shen ◽  
Marzieh Taghavi ◽  
Heike Münzberg ◽  
Roy J Martin ◽  
...  
Keyword(s):  
Amino Acid ◽  
Food Intake ◽  
Feeding Behavior ◽  
Control Diet ◽  
Peripheral Tissues ◽  
Protein Status ◽  
Branched Chain Amino Acid ◽  
Branched Chain ◽  
Branched Chain Aminotransferase ◽  
Deficient Mice

Elevation of dietary or brain leucine appears to suppress food intake via a mechanism involving mechanistic target of rapamycin, AMPK, and/or branched chain amino acid (BCAA) metabolism. Mice bearing a deletion of mitochondrial branched chain aminotransferase (BCATm), which is expressed in peripheral tissues (muscle) and brain glia, exhibit marked increases in circulating BCAAs. Here, we test whether this increase alters feeding behavior and brain neuropeptide expression. Circulating and brain levels of BCAAs were increased two- to four-fold in BCATm-deficient mice (KO). KO mice weighed less than controls (25.9 vs 20.4 g,P<0.01), but absolute food intake was relatively unchanged. In contrast to wild-type mice, KO mice preferred a low-BCAA diet to a control diet (P<0.05) but exhibited no change in preference for low- vs high-protein (HP) diets. KO mice also exhibited low leptin levels and increased hypothalamicNpyandAgrpmRNA. Normalization of circulating leptin levels had no effect on either food preference or the increasedNpyandAgrpmRNA expression. If BCAAs act as signals of protein status, one would expect reduced food intake, avoidance of dietary protein, and reduction in neuropeptide expression in BCATm-KO mice. Instead, these mice exhibit an increased expression of orexigenic neuropeptides and an avoidance of BCAAs but not HP. These data thus suggest that either BCAAs do not act as physiological signals of protein status or the loss of BCAA metabolism within brain glia impairs the detection of protein balance.

Effect of season and dietary fibre on feeding behaviour of lactating sows in a tropical climate

2003 ◽  
Vol 77 (3) ◽  
pp. 429-437 ◽  
Author(s):  
D. Renaudeau ◽  
J.-L. Weisbecker ◽  
J. Noblet
Keyword(s):  
Food Intake ◽  
Dietary Fibre ◽  
Feeding Behaviour ◽  
Control Diet ◽  
Warm Season ◽  
Tropical Climate ◽  
Large White ◽  
Significant Difference ◽  
Lactating Sows ◽  
Hot Season

AbstractTwenty-seven multiparous Large White sows were used to determine the effect of season in a tropical climate and dietary fibre on their feeding behaviour during lactation. The experiment was conducted in Guadeloupe (French West Indies, latitude 16°N, longitude 61°W) between October 1999 and January 2001; climatic conditions in the farrowing room were equivalent to outdoor conditions. Two seasons were determined a posteriori from climatic criteria recorded continuously in the farrowing room. During the warm season, ambient temperature and relative humidity averaged 25°C and 0·868, respectively. The corresponding values for the hot season were 27·5°C and 0·835. Experimental diets offered during lactation were a control diet (C; 140 g neutral-detergent fibre (NDF) per kg) and a high fibre diet (HF; 200 g NDF per kg). Sows were offered food ad libitum between the 6th and the 27th day of lactation. Daily food intake between day 6 and day 27 decreased during the hot season (P < 0·001; 3226 v. 5571 g/d during the warm season). This was achieved by a reduction of both meal size (P < 0·05; 460 v. 718 g per meal) and ingestion and consumption time (P < 0·01; -11·1 and -15·3 min/day, respectively) whereas the number of meals remained constant (8·4 meals per day on average). During warm season, hourly food intake peaked twice daily near sunrise and sunset. During the hot season, peaks were attenuated and food intake was reduced during the hotter periods of the day and increased during the fresher period of the day, especially in early morning. As a result the diurnal partition of food intake was significantly affected by season; proportionately 0·62 and 0·47 of total food intake occurred during the day in warm and in hot seasons, respectively. Standing duration averaged 138 min/ day with no significant difference between seasons. Feeding behaviour criteria were not influenced by diet composition. In conclusion, the season in a humid tropical climate significantly affects the feeding behaviour of lactating sows.

scholarly journals Effects of a high-fat-diet supplemented with probiotics and ω3-fatty acids on appetite regulatory neuropeptides and neurotransmitters in a pig model

2020 ◽  
Vol 11 (4) ◽  
pp. 347-359
Author(s):  
D. Valent ◽  
L. Arroyo ◽  
E. Fàbrega ◽  
M. Font-i-Furnols ◽  
M. Rodríguez-Palmero ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Animal Model ◽  
Weight Gain ◽  
Food Intake ◽  
High Fat Diet ◽  
Control Diet ◽  
Omega 3 Fatty Acids ◽  
Omega 3 ◽  
High Fat ◽  
Brain Functions

The pig is a valuable animal model to study obesity in humans due to the physiological similarity between humans and pigs in terms of digestive and associated metabolic processes. The dietary use of vegetal protein, probiotics and omega-3 fatty acids is recommended to control weight gain and to fight obesity-associated metabolic disorders. Likewise, there are recent reports on their beneficial effects on brain functions. The hypothalamus is the central part of the brain that regulates food intake by means of the production of food intake-regulatory hypothalamic neuropeptides, as neuropeptide Y (NPY), orexin A and pro-opiomelanocortin (POMC), and neurotransmitters, such as dopamine and serotonin. Other mesolimbic areas, such as the hippocampus, are also involved in the control of food intake. In this study, the effect of a high fat diet (HFD) alone or supplemented with these additives on brain neuropeptides and neurotransmitters was assessed in forty-three young pigs fed for 10 weeks with a control diet (T1), a high fat diet (HFD, T2), and HFD with vegetal protein supplemented with Bifidobacterium breve CECT8242 alone (T3) or in combination with omega-3 fatty acids (T4). A HFD provoked changes in regulatory neuropeptides and 3,4-dihydroxyphenylacetic acid (DOPAC) in the hypothalamus and alterations mostly in the dopaminergic system in the ventral hippocampus. Supplementation of the HFD with B. breve CECT8242, especially in combination with omega-3 fatty acids, was able to partially reverse the effects of HFD. Correlations between productive and neurochemical parameters supported these findings. These results confirm that pigs are an appropriate animal model alternative to rodents for the study of the effects of HFD on weight gain and obesity. Furthermore, they indicate the potential benefits of probiotics and omega-3 fatty acids on brain function.

scholarly journals Dopamine Release Neuroenergetics in Mouse Striatal Slices

2020 ◽  
Author(s):  
Msema Msackyi ◽  
Yuanxin Chen ◽  
Wangchen Tsering ◽  
Ninghan Wang ◽  
Jingyu Zhao ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Nucleus Accumbens ◽  
Oxidative Phosphorylation ◽  
Neurodegenerative Disorder ◽  
Dorsal Striatum ◽  
Striatal Slices ◽  
Axonal Projections ◽  
Specific Vulnerability ◽  
Da Release

AbstractParkinson’s disease (PD) is the second most common neurodegenerative disease. Dopamine (DA) neurons in the substantia nigra par compacta with axonal projections to the dorsal striatum (dSTR) degenerate in PD while in contrast, DA neurons in the ventral tegmental area with axonal projections to the ventral striatum including the nucleus accumbens (NAcc) shell, are largely spared. To understand the pathogenesis of PD, it is important to study the neuroenergetics of DA neurons. This study aims to uncover the relative contribution of glycolysis and oxidative phosphorylation (OxPhos) to evoked DA release in the striatum. We measured evoked DA release in mouse striatal brain slices by fast-scan cyclic voltammetry every 2 minutes. Blocking OxPhos caused a greater reduction in evoked DA release in the dSTR compared to the NAcc shell, and blocking glycolysis caused a greater reduction in evoked DA release in the NAcc shell than in the dSTR. Furthermore, when glycolysis was bypassed in favor of direct OxPhos, evoked DA release in the NAcc shell was decreased by ∼50% over 40 minutes whereas evoked DA release in the dSTR was largely unaffected. These results demonstrated that the dSTR relies primarily on OxPhos for energy production to maintain evoked DA release whereas the NAcc shell relies more on glycolysis. Using two-photon imaging, we consistently found that the oxidation level of the DA terminals was higher in the dSTR than in the NAcc shell. Together, these findings partially explain the specific vulnerability of DA terminals in the dSTR to degeneration in PD.Significant statementThe neuroenergetics of dopaminergic neuron is important to understand Parkinson’s disease (PD), a neurodegenerative disorder associated with mitochondrial dysfunctions. However, the relative contributions of glycolysis and oxidative phosphorylation (OxPhos) to presynaptic energy demands in DA terminals are unclear. We addressed this question by measuring DA release in the dorsal striatum and nucleus accumbens (NAcc) shell of mouse brain using FSCV under reagents blocking different energy systems. We found that the NAcc shell relies on both glycolysis and OxPhos to maintain DA release while the dSTR relies heavily on OxPhos. We demonstrate the different neuroenergetics of DA terminals in these two brain areas, providing new fundamentally important insight into the specific vulnerability of DA terminals in the dSTR to degeneration in PD.

Sign in / Sign up

Export Citation Format

Share Document