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What markers track thermogenesis?

Thermogenesis is the production of heat through metabolic processes. This page outlines research markers used to track thermogenesis, including core body temperature, indirect calorimetry, and molecular indicators in adi

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What markers track thermogenesis?

Thermogenesis refers to the production of heat through metabolic processes, primarily in brown adipose tissue (BAT) and as a component of energy expenditure. In research settings, thermogenesis is tracked using a combination of physiological, biochemical, and molecular markers. These include core body temperature, oxygen consumption (VO2), carbon dioxide production (VCO2), respiratory exchange ratio (RER), and the expression or abundance of thermogenic proteins such as uncoupling protein 1 (UCP1) in adipose tissue. Additionally, non-shivering thermogenesis can be assessed via indirect calorimetry and infrared thermography. The specific markers employed depend on the model system (e.g., rodents, humans) and the research question.

The work centres on the sympathetic nervous system and its regulation of adipose tissue thermogenesis, particularly through beta-adrenergic receptor signalling and downstream effectors like UCP1.

Research Studies

FSTL1 and white adipose tissue browning in male mice

Follistatin-like 1 (FSTL1) is an adipokine that has been implicated in white adipose tissue (WAT) browning and thermogenesis. In male mice at ambient room temperature, overexpression of FSTL1 induced WAT browning, enhanced energy metabolism, and promoted glucose uptake. Mice with FSTL1 deficiency exhibited cold intolerance and were prone to obesity. Overexpression of FSTL1 specifically in WAT prevented metabolic dysfunction in mice with diet-induced obesity. However, FSTL1 could not directly induce thermogenesis in vitro, suggesting that its effects may be mediated through other factors [2].

Sulforaphane and thermogenesis in obesity models

Sulforaphane, an isothiocyanate derived from cruciferous vegetables, has been studied for its metabolic regulatory properties. A narrative review evaluated its effects in obesity and obesity-related metabolic dysfunction, noting its antioxidant, anti-inflammatory, and metabolic regulatory properties. The review critically assessed mechanistic insights, preclinical evidence, and clinical perspectives, but specific markers of thermogenesis were not detailed in the available evidence [3].

GIP receptor agonism and antagonism in obesity pharmacotherapy

Glucagon-like peptide-1 receptor (GLP-1R) agonists have transformed obesity pharmacotherapy, but their efficacy is limited by gastrointestinal adverse effects. Dual GLP-1R/glucose-dependent insulinotropic polypeptide (GIP) receptor agonists have shown clinical success, catalysing interest in GIP receptor modulation. The review discusses efficacy and tolerability of GIPR agonism and antagonism, but does not specify thermogenesis markers [4].

Systemic vibration therapy and thermogenesis in adults with obesity

A clinical trial evaluated the effects of Systemic Vibration Therapy (SVT) on thermogenesis, cardiovascular parameters, endocrine-inflammatory markers, and physical-functional performance in adults with obesity. The study compared two types of vibrating platforms (vertical and side-alternating) to a placebo group. The main questions included the effects of SVT on thermogenesis and physical-functional performance, as well as cardiovascular risk, hormone levels, and inflammation. However, the specific markers used to assess thermogenesis were not detailed in the available evidence [5].

Diet-induced thermogenesis and 24h energy expenditure

Diet-induced thermogenesis (DIT) is the energy expended for eating, absorbing, and processing nutrients. A clinical trial investigated how increasing caloric intake affects DIT and 24-hour energy expenditure in healthy adults aged 18 to 60 years. Participants stayed in a clinic for about 35 days and received 8 different diets, including 7 test diets. The study aimed to learn how different diets change DIT, but the specific markers used were not specified in the available evidence [6].

Postprandial gut hormone responses and meal-induced thermogenesis in type 1 diabetes

A study compared postprandial responses to a test meal between subjects with type 1 diabetes and healthy controls, focusing on gut hormone levels, meal-induced thermogenesis, hunger and satiety perception, and other metabolic parameters. The markers for thermogenesis were not detailed in the available evidence [7].

Long-term effects of weight loss on meal-induced thermogenesis

A study examined postprandial gut-hormone secretion, meal-induced thermogenesis, fasting plasma metabolomic/lipidomic and cardiovascular indices among surgically managed obese individuals in the long term compared to conservatively managed obese patients. The specific thermogenesis markers were not specified in the available evidence [8].

Mazdutide in type 2 diabetes and nonalcoholic fatty liver disease

A clinical trial evaluated the efficacy and safety of switching to mazdutide therapy in patients with type 2 diabetes mellitus (T2DM) and moderate-to-severe nonalcoholic fatty liver disease (NAFLD) who had achieved glycemic control. The study focuses on Chinese patients with T2DM, who are susceptible to visceral fat accumulation. However, thermogenesis markers were not mentioned in the available evidence [1].

Canagliflozin and adipocyte thermogenesis in vitro

Canagliflozin (CANA) exhibits anti-obesity effects in clinical practice, but its direct adipocyte-intrinsic functions are poorly understood. In 3T3-L1 preadipocytes, CANA promoted differentiation and enhanced lipid mobilization and thermogenesis through AMPK/autophagy-dependent mechanisms. This suggests that CANA may influence thermogenic pathways in adipose tissue, but the specific markers used were not detailed in the available evidence [9].

Forskolin and de novo beige adipogenesis

Forskolin, delivered locally to adipose stem cells, induced de novo beige adipogenesis and adipose tissue browning to combat obesity. This approach aims to overcome off-target effects and poor durability of current browning inducers. The specific thermogenesis markers were not specified in the available evidence [10].

EGCG and BAT-independent thermogenic switch

Epigallocatechin gallate (EGCG) has anti-obesity effects and may trigger a BAT-independent thermogenic switch and remodel the immune microenvironment in subcutaneous adipose tissue. The study investigated whether EGCG can trigger adaptive thermogenesis, but the specific markers were not detailed in the available evidence [11].

Time-restricted feeding and HIIT in diabetic rats

A study evaluated the independent and combined effects of time-restricted feeding (TRF) and high-intensity interval training (HIIT) on thermogenesis-related protein abundance in white adipose tissue of diabetic rats. Forty male Wistar rats were divided into normal and diabetic groups. The specific thermogenesis-related proteins were not detailed in the available evidence [12].

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