Understanding Brown Adipose Tissue (BAT) and Thermogenesis

What is brown fat? 

Humans have at least two main types of adipose tissue: energy‑storing white adipose tissue and heat‑producing brown adipose tissue (BAT).  Brown fat cells contain numerous mitochondria and express uncoupling protein‑1 (UCP1).  When activated (e.g., by sympathetic nerve stimulation), UCP1 uncouples oxidative phosphorylation so that energy from fatty acids and glucose is released as heat rather than being stored.  This “non‑shivering thermogenesis” allows mammals to maintain body temperature in cold environments without shivering.  Although BAT was once thought to disappear after infancy, positron‑emission tomography/computed tomography (PET‑CT) studies have shown metabolically active BAT in adult humans; its activity is higher during cold exposure and suppressed by β‑blockers.

Cold → more BAT activity

• When you get cold, your body activates the sympathetic nervous system (SNS).

• SNS nerves release noradrenaline onto brown fat.

• Noradrenaline binds to β-adrenergic receptors (especially β3) on brown fat cells.

• This triggers UCP1 in the mitochondria → brown fat burns fatty acids and glucose to make heat (non-shivering thermogenesis).

• Result: BAT activity goes up during cold exposure.

β-blockers → less BAT activity

• β-blockers (like propranolol, bisoprolol etc.) block β-adrenergic receptors.

• If those receptors are blocked, noradrenaline can’t signal properly to brown fat.

• With the “on” switch blocked, brown fat can’t activate UCP1 as strongly, so it burns less fuel for heat.

• Result: BAT activity is reduced/suppressed in people taking β-blockers, even if they’re exposed to cold.

• Cold = presses the gas pedal (SNS → β-receptors → more BAT thermogenesis).

• β-blockers = put a block under the gas pedal (less response to SNS → lower BAT activity).

Where is it located? 

In adults, BAT is primarily found in the supraclavicular and neck regions, near the spine and kidneys.  Some white fat depots can acquire a BAT‑like phenotype (“beige” fat) under certain conditions, adding to the body’s thermogenic capacity .

Why Brown Fat Thermogenesis Matters for Health and Weight

Thermogenesis in BAT consumes substrates (free fatty acids and glucose) and elevates energy expenditure.  Evidence from human experiments suggests several potential health benefits:

• Increased energy expenditure and improved metabolism.  During acute cold exposure, BAT glucose uptake and fatty‑acid oxidation increase dramatically.  In a small PET‑CT study, cold exposure raised energy expenditure about 1.8‑fold and BAT took up both glucose and non‑esterified fatty acids from the bloodstream.  The study estimated that BAT accounted for ~1.3 % of plasma glucose turnover and ~0.25 % of plasma free‑fatty‑acid turnover during cold exposure.

• Improved insulin sensitivity.  A landmark experiment showed that 10 days of cold acclimation (~14–15 °C) increased non‑shivering thermogenesis and significantly improved skeletal‑muscle insulin sensitivity by ~43 % in patients with type 2 diabetes.  Later, a randomised crossover study exposed healthy volunteers to 15–16 °C for 6 h/day over 10 days; non‑shivering thermogenesis increased from ~10.8 % to 17.8 % and the amount of PET‑detectable BAT increased.

• Better postprandial glucose control and lipid profiles.  Another trial acclimated healthy adults to a cooler environment overnight (19 °C) for two months.  Postprandial insulin levels after a mixed meal were lower while glucose levels remained unchanged, indicating improved insulin sensitivity; adiponectin increased and leptin decreased .

  
  

Strategies to Increase Brown Fat Thermogenesis

Cold Exposure and Acclimation

• Short‑term cold exposure.  Wearing light clothing in a cool environment (~15–19 °C) for a few hours stimulates BAT and can burn extra calories.  In healthy volunteers, a 10‑day acclimation increased non‑shivering thermogenesis and BAT volume.

• Prolonged cold acclimation.  Sleeping in a cool bedroom (19 °C) for several weeks improved insulin sensitivity and increased adiponectin while decreasing leptin levels.  However, mild cold exposure without shivering (16–17 °C) in older patients did not improve insulin sensitivity , suggesting that some degree of cold‑induced muscle activation is necessary.

• Practical tips: Gradually lower your living or sleeping environment temperature (to ~19 °C), take cool showers, or spend time outside in cold weather.  Avoid prolonged discomfort or hypothermia and consult a physician if you have cardiovascular issues.

Diet and Bioactive Compounds

• Capsaicin and capsinoids.  Capsaicin (the compound that makes chili peppers hot) and its non‑pungent analogs (capsinoids) activate transient receptor potential vanilloid 1 (TRPV1) channels, stimulating the sympathetic nervous system.  Acute capsinoid ingestion increases resting energy expenditure only in individuals with active BAT, while prolonged ingestion may recruit BAT.  A randomised double‑blind trial in middle‑aged men who took dihydrocapsiate (9 mg/day) for six weeks showed increased BAT vascular density (measured via near‑infrared spectroscopy).  Changes in BAT‑density correlated with resting energy expenditure, and in overweight participants REE increased by 4.3 % (vs. –2.1 % in the placebo group).

• Other dietary factors.  Research is ongoing on certain foods (e.g., green tea catechins, fish‑oil–derived omega‑3s) that might enhance BAT activity by stimulating the sympathetic nervous system, but human evidence is limited.  Consuming adequate protein and balancing energy intake remain critical for weight management.

Exercise and Lifestyle

• Exercise.  Surprisingly, long‑term moderate or vigorous exercise does not seem to increase BAT volume or activity.  The ACTIBATE randomised trial found no significant differences in BAT volume or FDG uptake after 24 weeks of moderate or vigorous exercise compared with control .  Nevertheless, exercise improves overall energy balance, muscle insulin sensitivity and cardiovascular health, and should remain part of any weight‑loss plan.

• Adequate sleep and circadian rhythm.  Brown fat is influenced by circadian clocks and thyroid hormones; maintaining a regular sleep schedule and addressing thyroid disorders can support metabolic health.

• Avoiding thermoneutral comfort all the time.  Spending all day at thermoneutral temperatures (22–24 °C) may reduce BAT activity.  Incorporating mild cold exposure in daily life could help maintain BAT function.

Key takeaways

• Brown fat is a metabolically active tissue that burns calories to generate heat and may support better blood sugar, lipids and overall metabolic health.

• Human trials show that cold exposure, capsinoid supplements and β3-adrenergic drugs can activate brown fat and slightly increase energy expenditure, with some improvements in insulin sensitivity and cholesterol – but they are not magic bullets.

• For most of people, the most realistic strategy is to layer gentle brown-fat-friendly habits on top of a solid foundation of nutrition, movement and sleep:

  
  

  • Comfortable cooler environments rather than heavy heating

  • Protein-rich, whole-food meals with spices and green tea

  • Regular strength and aerobic exercise

  • Good sleep and stress management

  
  

  
  

If you’d like guidance applying these ideas to your own body and lifestyle, book a consultation and we’ll work together on a realistic plan for healthy weight loss and long-term metabolic health.

References:

• Fuse, S. et al. (2020) ‘Effects of Capsinoid Intake on Brown Adipose Tissue Vascular Density and Resting Energy Expenditure in Healthy, Middle-Aged Adults: A Randomized, Double-Blind, Placebo-Controlled Study’, Nutrients, 12(9), p. 2676. Available at: https://doi.org/10.3390/nu12092676.

• Lans, A.A.J.J. van der et al. (2013) ‘Cold acclimation recruits human brown fat and increases nonshivering thermogenesis’, The Journal of Clinical Investigation, 123(8), pp. 3395–3403. Available at: https://doi.org/10.1172/JCI68993.

• Lee, P. et al. (2014) ‘Temperature-Acclimated Brown Adipose Tissue Modulates Insulin Sensitivity in Humans’, Diabetes, 63(11), pp. 3686–3698. Available at: https://doi.org/10.2337/db14-0513.

• Martinez-Tellez, B. et al. (2022) ‘No evidence of brown adipose tissue activation after 24 weeks of supervised exercise training in young sedentary adults in the ACTIBATE randomized controlled trial’, Nature Communications, 13(1), p. 5259. Available at: https://doi.org/10.1038/s41467-022-32502-x.

• O’Mara, A.E. et al. (2020) ‘Chronic mirabegron treatment increases human brown fat, HDL cholesterol, and insulin sensitivity’, The Journal of Clinical Investigation, 130(5), pp. 2209–2219. Available at: https://doi.org/10.1172/JCI131126.

• Ouellet, V. et al. (2012) ‘Brown adipose tissue oxidative metabolism contributes to energy expenditure during acute cold exposure in humans’, The Journal of Clinical Investigation, 122(2), pp. 545–552. Available at: https://doi.org/10.1172/JCI60433.

• Remie, C.M.E. et al. (2021) ‘Metabolic responses to mild cold acclimation in type 2 diabetes patients’, Nature Communications, 12, p. 1516. Available at: https://doi.org/10.1038/s41467-021-21813-0.

• Tanaka, R. et al. (2020) ‘Vigorous-Intensity Physical Activities Are Associated with High Brown Adipose Tissue Density in Humans’, International Journal of Environmental Research and Public Health, 17(8), p. 2796. Available at: https://doi.org/10.3390/ijerph17082796.

• Yoneshiro, T. et al. (2013) ‘Recruited brown adipose tissue as an antiobesity agent in humans’, The Journal of Clinical Investigation, 123(8), pp. 3404–3408. Available at: https://doi.org/10.1172/JCI67803.

• Yoneshiro, T. et al. (2025) ‘Brown fat thermogenesis and cold adaptation in humans’, Journal of Physiological Anthropology, 44, p. 11. Available at: https://doi.org/10.1186/s40101-025-00391-w.