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Hedi Raizer

Journal 4 min read

How Brown Adipose Tissue Changes with Age

Brown adipose tissue (BAT) function declines with age in humans, and the mechanisms behind that decline are an active area of research. This page summarises what laboratory and clinical studies have reported on BAT agein

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Brown adipose tissue (BAT), also called brown fat, is a thermogenic adipose depot whose adipocytes contain multiple lipid droplets and dense mitochondria expressing uncoupling protein 1 (UCP1). In adult humans, BAT functionality declines with age, and this decline is one proposed contributor to unhealthy weight gain, particularly central obesity [6]. The formal question this page addresses is what changes in BAT with age and what mechanisms have been proposed for that change.

Most of the mechanistic work in this area centres on the TGF-β superfamily and its downstream SMAD signalling, together with adrenergic and NAD+-dependent pathways [1][2][3][6].

Research Studies

NAD+ availability and human BAT function with age

A registered clinical study is examining whether declining nicotinamide adenine dinucleotide (NAD+) availability contributes to the age-related loss of brown fat metabolism in human adults. The study notes that the reasons for the decline in brown fat functionality with age are not clearly understood, and that NAD+ is central to several metabolic processes. The project is designed to clarify whether NAD+-based molecules play a role in that decline [6].

FSTL1 and white adipose tissue browning in mice

Follistatin-like 1 (FSTL1) is an adipokine reported to be essential for white adipose tissue (WAT) adipogenesis, brown adipose tissue involution, and thermogenesis. In male mice at ambient room temperature, FSTL1 overexpression induced WAT browning, enhanced energy metabolism, and promoted glucose uptake. Overexpression of FSTL1 specifically in WAT prevented metabolic dysfunction in mice with diet-induced obesity, while FSTL1-deficient mice exhibited cold intolerance and were prone to obesity. FSTL1 could not directly induce the browning response on its own, indicating an indirect mechanism [1].

Follistatin and adipose browning in atherosclerosis models

Follistatin (FST) binds and neutralises members of the TGF-β superfamily, regulating skeletal muscle, adipose, and bone homeostasis. FST promotes adipose browning and enhances energy metabolism in mice, with improved plasma lipid profiles. Transcriptomic and metabolomic analysis of the Hybrid Mouse Diversity Panel found that Fst expression was negatively correlated with aortic lesion area, prompting investigation of its anti-atherogenic potential in the context of BAT activation [2].

GDF-11 and cold-induced browning

Growth differentiation factor 11 (GDF-11) is a circulating TGF-β superfamily member. In mice exposed to cold to induce browning, GDF-11 expression and SMAD2/3 activation were assessed in BAT, visceral and subcutaneous WAT, and skeletal muscle. The study combined in vivo results with in vitro approaches using 3T3-L1 cells [3].

Erythropoietin and adipose lipid handling

Erythropoietin (EPO) is best known as a regulator of erythrocyte production, but it also influences non-hematopoietic tissues including adipose tissue, skeletal muscle, and liver. EPO enhances lipolysis while inhibiting lipogenic gene expression in white adipose tissue, brown adipose tissue, and skeletal muscle, and plays a role in maintaining metabolic homeostasis and regulating fat mass [5].

Beta3-adrenergic receptor agonism and BAT adaptation

A clinical study is investigating the physiological responses and adaptation of BAT to chronic treatment with beta3-adrenergic receptor agonists in adults aged 18–40 with a body mass index between 18 and 40. The study notes that BAT may prevent weight gain, improve insulin sensitivity, and reduce fatty liver, and aims to learn more about how BAT works to burn energy [7].

Thyroid hormones and BAT amount and activity

An observational study is evaluating the effect of thyroid hormones on BAT in humans with thyrotoxicosis, using FDG-PET/CT, indirect calorimetry, and fat biopsies in the acute phase and again in the euthyroid phase after treatment. The hypothesis under test is that high circulating T3 levels affect the amount and function of BAT [8].

Capsinoid supplementation and BAT in obese adolescents

A clinical study is examining capsinoid supplementation and BAT in obese adolescents. The background notes that interest in BAT has increased following the discovery of functional BAT in humans, and that BAT is specialised for energy expenditure through heat production via oxidation of fatty acids in brown adipocytes. Cold exposure is described as the major physiological stimulus for BAT activation [4].

EGCG and BAT-independent thermogenesis

Epigallocatechin gallate (EGCG) has reported anti-obesity effects, and work in this area has examined whether it triggers a BAT-independent thermogenic switch and remodels the immune microenvironment in subcutaneous adipose tissue. The efficacy of adaptive thermogenesis as a therapeutic approach is limited by low BAT activity, which is the context for this line of investigation [9].

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