Scientists discovered that two types of brain cells in a reward center called the nucleus accumbens control how much high-fat food we eat—but they work differently depending on whether you’re male or female. Using advanced techniques to activate and deactivate these cells in mice, researchers found that one type of cell (D1) suppresses junk food eating in males, while another type (D2) actually increases eating in females. This discovery suggests that obesity treatments might need to be tailored differently for men and women based on how their brains respond to tempting foods.
The Quick Take
- What they studied: How two specific types of brain cells control the urge to eat high-fat foods, and whether this control works the same way in males and females
- Who participated: Male and female laboratory mice that were given access to high-fat food while researchers controlled their brain cell activity
- Key finding: One brain cell type (D1) reduces junk food eating in males when activated, while a different cell type (D2) increases eating in females when activated—suggesting sex-based differences in how our brains control food cravings
- What it means for you: Future obesity treatments might work better if they’re designed differently for men versus women, targeting the specific brain cells that control food cravings in each sex. However, this research is in mice, so human studies are needed before applying these findings to people
The Research Details
Researchers used three advanced techniques to study brain cell activity in mice. First, they used optogenetics—a method where special light activates or deactivates specific brain cells. Second, they used chemogenetics—a technique where drugs activate or deactivate targeted cells. Third, they used fiber photometry—a method that measures brain cell activity in real-time while mice eat. The researchers focused on two types of cells in the nucleus accumbens (a brain region involved in reward and motivation): D1-expressing cells and D2-expressing cells. They compared how these cells behaved differently in male versus female mice when given access to high-fat food.
The study was designed to establish a direct cause-and-effect relationship between specific brain cell activity and eating behavior. By turning cells on and off and measuring the results, the researchers could prove which cells actually control food intake, rather than just observing correlations. This approach is more powerful than simply watching what happens naturally.
This research matters because obesity is a major health problem partly caused by our brains’ reward systems making us crave unhealthy foods. Previous research suggested these two cell types had opposite effects, but nobody had proven it directly or discovered that males and females might respond differently. Understanding the exact brain mechanisms that drive overeating could lead to better, more targeted treatments. The sex-specific findings are particularly important because most medical treatments are developed without considering that men and women might have different biological responses.
This study was published in The Journal of Neuroscience, a highly respected scientific journal. The researchers used multiple complementary techniques (optogenetics, chemogenetics, and fiber photometry) to verify their findings, which strengthens confidence in the results. The study was conducted in a controlled laboratory setting with genetically modified mice designed specifically for this type of research. However, because the study used mice rather than humans, results may not directly apply to people. The sample size for individual experiments wasn’t specified in the abstract, which is a limitation for assessing statistical power.
What the Results Show
When researchers activated D1 brain cells using light or drugs, mice ate significantly less high-fat food. Interestingly, this effect was stronger in male mice. When they deactivated D1 cells, male mice ate more junk food, but female mice showed little change—suggesting D1 cells primarily control eating in males.
The opposite pattern emerged for D2 cells. Activating D2 cells increased high-fat food consumption, but only in female mice. When D2 cells were deactivated, both male and female mice ate less, though the effect was more pronounced in females. This suggests D2 cells play a larger role in driving food cravings in females.
Using real-time brain activity monitoring, researchers observed that D2 cell activity increased over repeated exposures to high-fat food in female mice, and this increasing activity correlated with eating more and more food. This pattern wasn’t observed in males, further supporting sex-based differences in how these cells work.
The research revealed that the brain’s reward system doesn’t work the same way in males and females when it comes to food motivation. The findings suggest that experience matters—repeated exposure to high-fat food changes how these brain cells respond, particularly in females. This could explain why some people develop stronger cravings for unhealthy foods over time. The dynamic nature of D2 cell activity suggests these cells might be involved in learning and habit formation around food, not just immediate eating decisions.
Earlier research suggested that D1 and D2 cells have opposite roles in reward processing, but this study provides direct proof of that opposition specifically for food intake. Previous work didn’t clearly establish sex-based differences in these mechanisms. This research builds on decades of neuroscience showing that the nucleus accumbens is crucial for reward-driven behavior, but adds important nuance by showing that the two main cell types don’t just have opposite effects—they have sex-specific effects. This finding challenges the assumption that male and female brains process food rewards identically.
The study used mice, not humans, so results may not directly translate to people. Mice have simpler brains and different social environments than humans, which could affect how these brain mechanisms work. The research focused only on high-fat food, so it’s unclear whether these findings apply to other types of palatable or unhealthy foods. The study didn’t examine how factors like stress, sleep, or hormonal cycles might influence these brain cells’ effects on eating. Additionally, the specific sample sizes for individual experiments weren’t provided, making it difficult to assess the statistical reliability of each finding. The research also didn’t test any potential treatments, so it’s unknown whether targeting these cells would actually help people lose weight or reduce cravings.
The Bottom Line
Based on this research, future obesity treatments should consider sex-based differences in brain reward systems (moderate confidence level—this is early-stage research). Potential approaches might include developing drugs that specifically target D1 cells in men or D2 cells in women. However, these are preliminary findings in mice, and human clinical trials would be needed before any new treatments could be recommended. Currently, standard obesity treatments like diet, exercise, and behavioral therapy remain the evidence-based approaches for all people.
This research is most relevant to people struggling with obesity or food cravings, particularly those who find it difficult to resist high-fat or palatable foods despite wanting to eat healthier. It’s also important for researchers developing new obesity treatments and for healthcare providers treating obesity. People with eating disorders or compulsive eating behaviors might find this research relevant. However, this is basic neuroscience research, not a clinical study, so it shouldn’t change anyone’s current treatment approach. If you’re struggling with weight or food cravings, consult with a healthcare provider about evidence-based treatments rather than waiting for treatments based on this research.
This is fundamental research establishing how brain cells control eating—it’s not a treatment study. It typically takes 5-10 years or more for basic neuroscience discoveries to lead to human clinical trials, and several more years for new treatments to become available. Don’t expect immediate practical applications. The value of this research is in guiding future treatment development, not in providing solutions you can use today.
Want to Apply This Research?
- Track daily high-fat food intake and cravings separately by sex-based patterns. Users could log: (1) times of day when cravings are strongest, (2) types of high-fat foods craved most, (3) whether cravings increase with repeated exposure to the same food, and (4) success rates of different coping strategies. This data could help identify personal patterns that might reflect the brain mechanisms described in this research.
- Implement a ‘craving awareness’ feature that helps users recognize when they’re experiencing hedonic (pleasure-based) eating versus homeostatic (hunger-based) eating. Users could set reminders to pause before eating high-fat foods and identify their motivation. The app could suggest sex-specific strategies: for males, emphasizing the ‘stop’ signal that D1 cells provide; for females, focusing on breaking the escalating pattern of repeated exposure that increases D2 cell activity.
- Create a long-term tracking dashboard showing: (1) weekly high-fat food consumption trends, (2) craving intensity ratings, (3) patterns in when cravings occur, and (4) effectiveness of different intervention strategies by sex. Include a feature to track whether cravings increase with repeated exposure to specific foods, which could indicate the D2 cell escalation pattern described in the research. Share anonymized data trends with users to help them understand their personal reward system patterns.
This research describes basic neuroscience findings in mice and does not represent a clinical treatment or medical advice. The study has not been tested in humans, and results may not directly apply to people. Do not change your diet, eating habits, or medical treatment based on this research. If you’re struggling with obesity, food cravings, or compulsive eating, consult with a healthcare provider or registered dietitian for evidence-based treatment options. This article is for educational purposes only and should not replace professional medical advice.