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 ◽  
...  

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.

Nutrients ◽  
2020 ◽  
Vol 12 (7) ◽  
pp. 2036 ◽  
Author(s):  
Kaichi Yoshizaki ◽  
Masato Asai ◽  
Taichi Hara

Obesity is characterized by massive adipose tissue accumulation and is associated with psychiatric disorders and cognitive impairment in human and animal models. However, it is unclear whether high-fat diet (HFD)-induced obesity presents a risk of psychiatric disorders and cognitive impairment. To examine this question, we conducted systematic behavioral analyses in C57BL/6J mice (male, 8-week-old) fed an HFD for 7 weeks. C57BL/6J mice fed an HFD showed significantly increased body weight, hyperlocomotion in the open-field test (OFT) and Y-maze test (YMZT), and impaired sucrose preference in the sucrose consumption test, compared to mice fed a normal diet. Neither body weight nor body weight gain was associated with any of the behavioral traits we examined. Working memory, as assessed by the YMZT, and anxiety-like behavior, as assessed by the elevated plus maze test (EPMT), were significantly correlated with mice fed an HFD, although these behavioral traits did not affect the entire group. These results suggest that HFD-induced obesity does not induce neuropsychiatric symptoms in C57BL/6J mice. Rather, HFD improved working memory in C57BL/6J mice with less anxiety, indicating that an HFD might be beneficial under limited conditions. Correlation analysis of individual traits is a useful tool to determine those conditions.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Gianluca Sighinolfi ◽  
Samantha Clark ◽  
Landry Blanc ◽  
Daniela Cota ◽  
Boutayna Rhourri-Frih

AbstractOverweight and obesity have been shown to significantly affect brain structures and size. Obesity has been associated with cerebral atrophy, alteration of brain functions, including cognitive impairement, and psychiatric diseases such as depression. Given the importance of lipids in the structure of the brain, here, by using 47 mice fed a high fat diet (HFD) with 60% calories from fat (40% saturated fatty acids) and 20% calories from carbohydrates and age-matched control animals on a normal chow diet, we examined the effects of HFD and diet-induced obesity on the brain lipidome. Using a targeted liquid chromatography mass spectrometry analysis and a non-targeted mass spectrometry MALDI imaging approach, we show that the relative concentration of most lipids, in particular brain phospholipids, is modified by diet-induced obesity (+ 40%of body weight). Use of a non-targeted MALDI-MS imaging approach further allowed define cerebral regions of interest (ROI) involved in eating behavior and changes in their lipid profile. Principal component analysis (PCA) of the obese/chow lipidome revealed persistence of some of the changes in the brain lipidome of obese animals even after their switch to chow feeding and associated weight loss. Altogether, these data reveal that HFD feeding rapidly modifies the murine brain lipidome. Some of these HFD-induced changes persist even after weight loss, implying that some brain sequelae caused by diet-induced obesity are irreversible.


2014 ◽  
Vol 644-650 ◽  
pp. 5239-5243
Author(s):  
Ming Lian ◽  
Yu Fang Jiang ◽  
Shi Dong Lv ◽  
Yi Long He ◽  
Jiang Sheng Zhou ◽  
...  

Obesity has become a fast growing epidemic in developing countries, as well as in some of the developing countries. Drinking Chinese tea has been demonstrated to have multiple beneficial effects to obese patients. It showed strong effect in reducing body fat and lowering blood sugar. This article tested the effect of instant Pu-erh ripe tea on weight loss in diet-induced obese (DIO) mice. The results demonstrated that instant Pu-erh ripe tea was be able to reduce the mouse weight dose-dependently. Its effect is stronger than that of L-carnitine, a weight loss drug currently on the market. Instant Pu-erh ripe tea also accelerated lipid metabolism and eased the high-fat diet-induced liver injury.


2014 ◽  
Author(s):  
Matthew J. Peloqiun ◽  
Dave Bridges

Inbred C57BL/6J mice have been used to study diet-induced obesity and the detrimental physiological effects associated with it. Little is understood about predictive factors that predispose an animal to weight gain. To address this, mice were fed a high fat diet, control diet or normal chow diet. Several measurements including pre-diet serum hormone levels and pre-diet body weight were analyzed, but these had limited predictive value regarding weight gain. However, baseline measurements of weight loss in response to food deprivation showed a strong negative correlation with high fat diet-induced weight gain. These data suggest that fasting-induced weight loss in adolescent mice is a useful predictor of diet-induced weight gain.


2014 ◽  
Vol 644-650 ◽  
pp. 5248-5251
Author(s):  
Ming Lian ◽  
Yu Fang Jiang ◽  
Shi Dong Lv ◽  
Yi Long He ◽  
Jiang Sheng Zhou ◽  
...  

Obesity is becoming a worldwide epidemic disease, and the incidence is increasing year by year. Drinking tea has been demonstrated to have multiple beneficial effects to obese patients. This article tested the effect of instant Pu-erh black tea on weight loss in diet-induced obese (DIO) mice. The results demonstrated that instant Pu-erh black tea was be able to reduce the mouse weight dose-dependently. Its effect is stronger than that of L-carnitine, a weight loss drug currently on the market. Instant Pu-erh black tea also accelerated lipid metabolism and eased the high-fat diet-induced liver injury.


eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Lisa R Beutler ◽  
Timothy V Corpuz ◽  
Jamie S Ahn ◽  
Seher Kosar ◽  
Weimin Song ◽  
...  

Body weight is regulated by interoceptive neural circuits that track energy need, but how the activity of these circuits is altered in obesity remains poorly understood. Here we describe the in vivo dynamics of hunger-promoting AgRP neurons during the development of diet-induced obesity in mice. We show that high-fat diet attenuates the response of AgRP neurons to an array of nutritionally-relevant stimuli including food cues, intragastric nutrients, cholecystokinin and ghrelin. These alterations are specific to dietary fat but not carbohydrate or protein. Subsequent weight loss restores the responsiveness of AgRP neurons to exterosensory cues but fails to rescue their sensitivity to gastrointestinal hormones or nutrients. These findings reveal that obesity triggers broad dysregulation of hypothalamic hunger neurons that is incompletely reversed by weight loss and may contribute to the difficulty of maintaining a reduced weight.


Author(s):  
LC Bollheimer ◽  
H Wobser ◽  
CE Wrede ◽  
A Schäffler ◽  
J Schölmerich ◽  
...  

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