Maternal high-fat intake alters presynaptic regulation of dopamine in the nucleus accumbens and increases motivation for fat rewards in the offspring

Neuroscience ◽  
2011 ◽  
Vol 176 ◽  
pp. 225-236 ◽  
Author(s):  
L. Naef ◽  
L. Moquin ◽  
G. Dal Bo ◽  
B. Giros ◽  
A. Gratton ◽  
...  
Keyword(s):  
Nucleus Accumbens ◽  
Fat Intake ◽  
High Fat ◽  
Presynaptic Regulation

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 Input-specific modulation of murine nucleus accumbens differentially regulates hedonic feeding

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Daniel J. Christoffel ◽  
Jessica J. Walsh ◽  
Boris D. Heifets ◽  
Paul Hoerbelt ◽  
Sophie Neuner ◽  
...  
Keyword(s):  
Nucleus Accumbens ◽  
Neural Circuit ◽  
Critical Role ◽  
Synaptic Strength ◽  
Fat Intake ◽  
High Fat ◽  
Cell Type Specific ◽  
Paraventricular Thalamus ◽  
Opposing Effects ◽  
Motivated Behaviors

AbstractHedonic feeding is driven by the “pleasure” derived from consuming palatable food and occurs in the absence of metabolic need. It plays a critical role in the excessive feeding that underlies obesity. Compared to other pathological motivated behaviors, little is known about the neural circuit mechanisms mediating excessive hedonic feeding. Here, we show that modulation of prefrontal cortex (PFC) and anterior paraventricular thalamus (aPVT) excitatory inputs to the nucleus accumbens (NAc), a key node of reward circuitry, has opposing effects on high fat intake in mice. Prolonged high fat intake leads to input- and cell type-specific changes in synaptic strength. Modifying synaptic strength via plasticity protocols, either in an input-specific optogenetic or non-specific electrical manner, causes sustained changes in high fat intake. These results demonstrate that input-specific NAc circuit adaptations occur with repeated exposure to a potent natural reward and suggest that neuromodulatory interventions may be therapeutically useful for individuals with pathologic hedonic feeding.

scholarly journals High-fat intake induced by mu-opioid activation of the nucleus accumbens is inhibited by Y1R-blockade and MC3/4R- stimulation

2010 ◽  
Vol 1350 ◽  
pp. 131-138 ◽  
Author(s):  
Huiyuan Zheng ◽  
R. Leigh Townsend ◽  
Andrew C. Shin ◽  
Laurel M. Patterson ◽  
Curtis B. Phifer ◽  
...  
Keyword(s):  
Nucleus Accumbens ◽  
Fat Intake ◽  
High Fat ◽  
Mu Opioid

scholarly journals Replacing a Palatable High-Fat Diet with a Low-Fat Alternative Heightens κ-Opioid Receptor Control over Nucleus Accumbens Dopamine

Nutrients ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 2341
Author(s):  
Conner W. Wallace ◽  
Nari S. Beatty ◽  
Sarah A. Hutcherson ◽  
Heather A. Emmons ◽  
Madison C. Loudermilt ◽  
...  
Keyword(s):  
Weight Loss ◽  
Nucleus Accumbens ◽  
High Fat Diet ◽  
Elevated Plus Maze ◽  
High Fat ◽  
Food Cravings ◽  
Fast Scan Cyclic Voltammetry ◽  
Diet Induced Obesity ◽  
Plus Maze ◽  
Weight Loss Interventions

Diet-induced obesity reduces dopaminergic neurotransmission in the nucleus accumbens (NAc), and stressful weight loss interventions could promote cravings for palatable foods high in fat and sugar that stimulate dopamine. Activation of κ-opioid receptors (KORs) reduces synaptic dopamine, but contribution of KORs to lower dopamine tone after dietary changes is unknown. Therefore, the purpose of this study was to determine the function of KORs in C57BL/6 mice that consumed a 60% high-fat diet (HFD) for six weeks followed by replacement of HFD with a control 10% fat diet for one day or one week. HFD replacement induced voluntary caloric restriction and weight loss. However, fast-scan cyclic voltammetry revealed no differences in baseline dopamine parameters, whereas sex effects were revealed during KOR stimulation. NAc core dopamine release was reduced by KOR agonism after one day of HFD replacement in females but after one week of HFD replacement in males. Further, elevated plus-maze testing revealed no diet effects during HFD replacement on overt anxiety. These results suggest that KORs reduce NAc dopamine tone and increase food-related anxiety during dietary weight loss interventions that could subsequently promote palatable food cravings and inhibit weight loss.

scholarly journals Molecular Characterization of PGC-1β (PPAR Gamma Coactivator 1β) and its Roles in Mitochondrial Biogenesis in Blunt Snout Bream (Megalobrama amblycephala)

2020 ◽  
Vol 21 (6) ◽  
pp. 1935 ◽  
Author(s):  
Kangle Lu ◽  
Tomas Policar ◽  
Xiaojun Song ◽  
Samad Rahimnejad
Keyword(s):  
Molecular Characterization ◽  
Mitochondrial Biogenesis ◽  
Phylogenetic Analyses ◽  
Ppar Gamma ◽  
Megalobrama Amblycephala ◽  
Fat Intake ◽  
High Fat ◽  
Blunt Snout Bream ◽  
Mitochondria Biogenesis

This study aimed at achieving the molecular characterization of peroxisome proliferator-activated receptor-gamma coactivator 1β (PGC-1β) and exploring its modulatory roles in mitochondria biogenesis in blunt snout bream (Megalobrama amblycephala). A full-length cDNA of PGC-1β was cloned from liver which covered 3110 bp encoding 859 amino acids. The conserved motifs of PGC-1β family proteins were gained by MEME software, and the phylogenetic analyses showed motif loss and rearrangement of PGC-1β in fish. The function of PGC-1β was evaluated through overexpression and knockdown of PGC-1β in primary hepatocytes of blunt snout bream. We observed overexpression of PGC-1β along with enhanced mitochondrial transcription factor A (TFAM) expression and mtDNA copies in hepatocytes, and its knockdown led to slightly reduced NRF1 expression. However, knockdown of PGC-1β did not significantly influence TFAM expression or mtDNA copies. The alterations in mitochondria biogenesis were assessed following high-fat intake, and the results showed that it induces downregulation of PGC-1β. Furthermore, significant decreases in mitochondrial respiratory chain activities and mitochondria biogenesis were observed by high-fat intake. Our findings demonstrated that overexpression of PGC-1β induces the enhancement of TFAM expression and mtDNA amount but not NRF-1. Therefore, it could be concluded that PGC-1β is involved in mitochondrial biogenesis in blunt snout bream but not through PGC-1β/NRF-1 pathway.

scholarly journals Impact of Fat Intake on Blood Glucose Control and Cardiovascular Risk Factors in Children and Adolescents with Type 1 Diabetes

Nutrients ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 2625
Author(s):  
Chiara Garonzi ◽  
Gun Forsander ◽  
Claudio Maffeis
Keyword(s):  
Risk Factors ◽  
Type 1 Diabetes ◽  
Cardiovascular Risk ◽  
Glycemic Control ◽  
Children And Adolescents ◽  
Cardiovascular Risk Factors ◽  
Specific Role ◽  
Fat Intake ◽  
High Fat

Nutrition therapy is a cornerstone of type 1 diabetes (T1D) management. Glycemic control is affected by diet composition, which can contribute to the development of diabetes complications. However, the specific role of macronutrients is still debated, particularly fat intake. This review aims at assessing the relationship between fat intake and glycemic control, cardiovascular risk factors, inflammation, and microbiota, in children and adolescents with T1D. High fat meals are followed by delayed and prolonged hyperglycemia and higher glycated hemoglobin A1c levels have been frequently reported in individuals with T1D consuming high amounts of fat. High fat intake has also been associated with increased cardiovascular risk, which is higher in people with diabetes than in healthy subjects. Finally, high fat meals lead to postprandial pro-inflammatory responses through different mechanisms, including gut microbiota modifications. Different fatty acids were proposed to have a specific role in metabolic regulation, however, further investigation is still necessary. In conclusion, available evidence suggests that a high fat intake should be avoided by children and adolescents with T1D, who should be encouraged to adhere to a healthy and balanced diet, as suggested by ISPAD and ADA recommendations. This nutritional choice might be beneficial for reducing cardiovascular risk and inflammation.

scholarly journals A substitution model of dietary manipulation is an effective means of optimising lipid profile, reducing C-reactive protein and increasing insulin-like growth factor-1

2004 ◽  
Vol 92 (5) ◽  
pp. 809-818 ◽  
Author(s):  
Adrian H. Heald ◽  
Cheryl Golding ◽  
Reena Sharma ◽  
Kirk Siddals ◽  
Sara Kirk ◽  
...  
Keyword(s):  
Growth Factor ◽  
Dietary Intervention ◽  
Short Interval ◽  
The Other ◽  
Fat Intake ◽  
Insulin Like Growth Factor ◽  
C Reactive Protein ◽  
High Fat ◽  
Substitution Model ◽  
Reactive Protein

There are two key methods in which fat intake may be manipulated; the ‘substitution model’ and the ‘reduction model’. However insufficient information is known about the mechanisms of dietary fat reduction in individuals who have successfully reduced their fat intake, to be clear as to which strategy offers the greatest chance of success. Our objective was to ascertain the most effective dietary intervention for improving cardiovascular risk profile. Eighty female volunteers (high fat consumers) were recruited. Each subject was randomly allocated into one of the following groups. Substitution of high-fat foods was made with reduced-fat products, by the reduction of high-fat foods, by a combination of substitution and reduction strategies, or no advice was given. Each intervention lasted 3 months. Anthropometric measures and fasting blood samples were taken at baseline and follow-up. The substitution intervention resulted in weight loss (mean −1.4 (95% CI −2.4, −0.2) kg) and reduced percentage body fat (mean −1.3 (95% CI −2.0, −0.5)%). There was no significant weight change with the other interventions. Fasting triacylglycerols (−0.2 (SEM 0.07) mM; P=0.04), cholesterol and C-reactive protein (CRP) levels (0.8 (SEM 0.2) mg/l; P=0.04) fell with the substitution intervention, but not with the other interventions. Insulin-like growth factor-1 increased with both substitution and reduction (P=0.02). There was no significant change in fasting insulin or glucose with any intervention. The substitution model of dietary intervention is effective even over a relatively short interval of time in reducing fasting total cholesterol, triacylglycerols and CRP. Although the group size for the present study was small and involved females only, it has significant implications for population intervention strategies.

Abstract 477: Chronic Baroreflex Activation Improves Baroreflex Control of Heart Rate In Obesity

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Radu Iliescu ◽  
Ionut Tudorancea ◽  
Eric Irwin ◽  
Thomas Lohmeier
Keyword(s):  
Heart Rate ◽  
Pulse Interval ◽  
Vagal Activity ◽  
Fat Intake ◽  
High Fat ◽  
Baroreflex Control ◽  
Systolic Blood Pressure Variability ◽  
Body Weight Increase ◽  
Obesity Hypertension ◽  
Fat Feeding

Impaired baroreflex control of heart rate (BRS) and attendant risk for cardiac arrhythmias are associated with sympathetically-mediated obesity hypertension. Since both global and renal-specific sympathoinhibition have sustained antihypertensive effects in obesity, we compared BRS in obese dogs subjected to 7 days of electrical baroreflex activation (BA) and, after recovery (REC), to bilateral surgical renal denervation (RDX). After control (C) measurements and 4 weeks of high fat diet, fat intake was reduced (RF) to maintain a body weight increase of ∼ 50%, which led to an increase in mean arterial pressure (MAP) from 100±2 to 117±3 mmHg and heart rate (HR) from 86±3 to 130±4 bpm. Obesity hypertension was associated with decreased sensitivity of 24h spontaneous BRS (determined by the sequence technique from daily beat-to-beat time series) and pulse interval (PI) variability (24h SD). While both BA and RDX abolished hypertension, only BA diminished tachycardia and normalized BRS, consequently improving HR variability. Short-term systolic blood pressure variability (5 min SD) also decreased with high fat feeding and was restored to control upon reduction of fat intake (RF) during established obesity hypertension, suggesting a vasoplegic effect of fat. These data suggest that in addition to the antihypertensive effects of sympathoinhibition, BA corrects cardiac baroreflex dysfunction in obesity hypertension, presumably by enhancing cardiac vagal activity. This in turn markedly improves depressed HR variability, a known risk factor for cardiac arrhythmic events.

Could parental high-fat intake program the reproductive health of male offspring? A review

2021 ◽  
pp. 1-8
Author(s):  
Marcela Nascimento Sertorio ◽  
Debora Estadella ◽  
Daniel Araki Ribeiro ◽  
Luciana Pellegrini Pisani
Keyword(s):  
Reproductive Health ◽  
Male Offspring ◽  
Fat Intake ◽  
High Fat
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