Brain neurons linked to reduced fat inflammation could influence obesity and heart health

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Researchers from Japan’s National Institute of Physiological Sciences have identified brain cells that can dampen inflammation in white adipose tissue, a factor linked to cardiovascular risk in obesity. The study, published in Cell Reports, expands our understanding of how brain circuits influence fat tissue and heart health.

In experiments with obese mice, the team showed that certain neurons in the hypothalamus, a brain region that governs hunger and metabolic balance, produce a protein called SF1. These SF1-expressing neurons appear to modulate inflammatory processes within white subcutaneous adipose tissue, a form of fat that serves primarily as an energy reservoir. The discovery suggests a neural pathway through which the brain can regulate fat tissue inflammation, with potential implications for metabolic and cardiovascular disease prevention.

According to the researchers, mice lacking SF1-expressing neurons tended to gain more weight when subjected to both standard and high-fat diets, underscoring the role of these neurons in maintaining energy balance and metabolic health. This finding aligns with broader evidence that brain signals can influence how fat tissue stores energy and responds to dietary challenges, which in turn can affect systemic inflammation and vascular risk.

Human fat exists in several forms. White adipose tissue is the predominant type, serving as a long-term energy store. Brown adipose tissue, by contrast, contributes to thermogenesis, generating heat by burning calories to support body temperature. Newer lines of inquiry have connected inflammation within white adipose tissue to higher risks of cardiovascular disease among people who are overweight or obese, highlighting a potential link between neural regulation of fat and heart health.

The neurons studied by the scientists may offer a route to novel therapies for obesity and related conditions. If researchers can learn to safely enhance the activity of SF1-expressing neurons or mimic their anti-inflammatory effects, it could lead to strategies that reduce white fat inflammation and lower cardiovascular risk without relying solely on diet or exercise measures alone.

It is worth noting that early clinical experiences with weight loss drugs have raised concerns about possible thyroid cancer risks in some cases. While that risk profile is a separate area of investigation, the current findings emphasize the value of exploring brain-based approaches to metabolic benefit and the broader health implications of fat tissue inflammation (Cell Reports, 2023).”,

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