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Chan, P.;  Hsieh, P. Mechanisms of Diet-Induced Thermogenesis. Encyclopedia. Available online: (accessed on 03 December 2023).
Chan P,  Hsieh P. Mechanisms of Diet-Induced Thermogenesis. Encyclopedia. Available at: Accessed December 03, 2023.
Chan, Pei-Chi, Po-Shiuan Hsieh. "Mechanisms of Diet-Induced Thermogenesis" Encyclopedia, (accessed December 03, 2023).
Chan, P., & Hsieh, P.(2022, October 24). Mechanisms of Diet-Induced Thermogenesis. In Encyclopedia.
Chan, Pei-Chi and Po-Shiuan Hsieh. "Mechanisms of Diet-Induced Thermogenesis." Encyclopedia. Web. 24 October, 2022.
Mechanisms of Diet-Induced Thermogenesis

Brown adipose tissue (BAT) has been considered a vital organ in response to non-shivering adaptive thermogenesis, which could be activated during cold exposure through the sympathetic nervous system (SNS) or under postprandial conditions contributing to diet-induced thermogenesis (DIT). Humans prefer to live within their thermal comfort or neutral zone with minimal energy expenditure created by wearing clothing, making shelters, or using an air conditioner to regulate their ambient temperature; thereby, DIT would become an important mechanism to counter-regulate energy intake and lipid accumulation. In addition, there has been a long interest in the intriguing possibility that a defect in DIT predisposes one to obesity and other metabolic diseases. 

diet-induced thermogenesis BAT regulatory mechanism obesity

1. Introduction

The thermogenic activity of Brown adipose tissue (BAT) is stimulated by cold and also by a meal that induced a parallel increase in heat production, which has been well-documented to resist obesity through facilitating adaptive thermogenesis and energy expenditure (EE) both in rodents and humans [1]. BAT possesses a higher capacity to metabolize glucose and fatty acids, promotes heat production and EE, and is characterized by multilocular small lipid droplets, high mitochondrial density, and the expression of key thermogenic protein-uncoupling protein 1 (UCP1). There is evidence supporting that BAT could significantly affect whole-body energy metabolism in rodents and humans [2][3]. Therefore, BAT activation has been considered a potential therapeutic target in the treatment of obesity and related diseases [4].
In humans and rodents, the resting metabolic rate (RMR) accounts for 60–70% of whole-body EE, which is required for the performance of cellular and organ functions [5][6]. RMR is majorly determined by fat-free mass in the body. In general, gender difference and aging are the two main physiological factors to affect RMR [7][8][9], which may be due to differences in fat-free mass, especially skeletal muscle [10]. DIT is the increase in EE associated with food intake [11] and accounts for 5–15% of total EE [12]. The magnitude of the thermic effect of food depends on diet composition and caloric intake. DIT represents about 10% of daily total EE in healthy subjects [11]. DIT also could be affected by oral stimuli (i.e., the duration of tasting food and chewing in the mouth) [13], and environmental factors [14].

2. Sympathetic Nervous System (SNS)–BAT Axis

CIT could be generated by activating SNS and inducing BAT thermogenesis through the β3-adrenergic receptor (ADRB3) in mice and β2-adrenergic receptor in humans [15]. Based on the principal role of the SNS-βAR axis for CIT, it is conceivable that this axis might also be a key mechanism in DIT. For instance, SNS activity in BAT calculated from tissue norepinephrine turnover rate is increased in mice with long-term cafeteria and high-calorie diet feeding [16][17]. In addition, studies [18] also showed that surgical denervation of BAT could significantly attenuate metabolic activation of BAT after intake of a liquid meal in rats. Accordingly, denervation of BAT also alleviates the increase in mitochondrial GDP binding, total UCP1 protein content, and mitochondrial content in rats on an energy-enriched diet [19]. These results support the content that BAT activation in DIT is, at least in part, mediated through SNS activation. Moreover, previous reports have further demonstrated that food palatability and oropharyngeal taste sensation are also substantially involved in diet-induced sympathetic activation and BAT thermogenesis [20][21][22].

3. Gut-Secreted Peptides and Hormones and Bile Acids

Since the release of gastrointestinal peptides is one of the acute physiological responses to eating, some of these peptides have been reported to act as mediators to regulate DIT. For instance, gut hormones could activate BAT through their effects on the efferent SNS tone, such as cholecystokinin (CCK) [23][24] and glucagon-like peptide (GLP-1) [25]. In addition, the study of Li et al. [26] revealed a novel endocrine gut–BAT–brain axis triggered by secretin that initiates the canonical secretin receptor (SCTR)–cAMP–PKA–lipolysis–UCP1 pathway in brown adipocytes from the intestine during a meal. Their observation supported that a postprandial increase in circulating secretin activates BAT thermogenesis by binding to SCTR in brown adipocytes. On the other hand, bile acids have been documented to activate BAT directly through Takeda G-protein receptor 5 (TGR5) in brown adipocytes [27]. Watanabe et al., [28] further demonstrated that bile acids activate TGR5 in mouse brown adipocytes and then, facilitate thermogenic activity through type 2 deiodinase (D2) activation. Accordingly, direct stimulatory effects of bile acids (chenodeoxycholic acid) on BAT activity have been evidenced in humans using brown adipocytes in vitro and using FDG-PET/CT scan in vivo [28][29]. TGR5 has also been demonstrated to participate in browning of white adipose tissue under cold exposure and prolonged HFD feeding [30]. Thereby, targeting TGR5–BAT axis with bile acids or drugs could be a promising target for combating obesity and related metabolic disorders in humans.

4. Insulin

It is well recognized that the role of insulin as a key hormone in the storage of ingested nutrients, and also possesses the capacity to modulate energy balance after a meal. A recent study has indicated that insulin is a crucial protein involved in the mitochondrial bioenergetic and thermogenic capacity of brown adipocytes [31]. In fact, BAT appears to be differently activated by insulin and cold. When activated by cold, it dissipates energy in a perfusion-dependent manner. Nevertheless, in response to insulin, BAT glucose uptake could have a 5-fold increase independently of its perfusion [32][33]. In addition, it is suggested that insulin may play an important role in the dietary induction of facilitative adaptive thermogenesis. For instance, the study conducted with ten healthy lean volunteers and a euglycemic clamp method in conjunction with respiratory exchange measurements, has shown the progressive increase in RMR along with the increase in the glucose infusion rate without changes in insulin and norepinephrine concentrations. It is implicated that insulin-stimulated glucose uptake is crucial for the thermogenic response of insulin [34]. On the other hand, Lee et al. have demonstrated that the recruitment of human BAT is accompanied by augmented DIT and postprandial insulin sensitivity [35]. Thus, it appears that the interactions between insulin and thermogenesis seen in rats could also exist in humans after meals.
Insulin resistance is a well-characterized consequence of obesity. Cafeteria diet feeding was conducted with normal and diabetic animals to assess changes in insulin-mediated glucose metabolism and to investigate the effects of insulin resistance on the development of DIT [36]. The attenuated DIT shown in cafeteria-fed diabetic rats was restored by an intensive program of insulin administration [36]. In addition, insulin resistance could result in a defect in insulin-mediated thermogenic response which contributes to the pathogenesis of obesity in humans [35]. The study of Aherne and Hull [37] conducted with human autopsy demonstrated that for obese infants of diabetic mothers exhibited impaired BAT function, further suggesting that maternal insulin deficiency may affect the thermogenic function of BAT in the offspring. Nevertheless, a recent report from Loeliger, R.C. has shown that DIT was not associated with BAT activity. DIT after an oral glucose load was not associated with stimulated 18F-FDG uptake into BAT, suggesting that DIT is independent of BAT activity caused by facilitating glucose uptake in humans [38]. The underlying mechanism of insulin on DIT is needed to be further clarified.

5. Liver-Derived Factors

Hepatic tissue has been documented to be involved to a significant extent in the thermogenesis process. The study was conducted with rats fed chow or a cafeteria diet of highly palatable human foods and measured the RMRs (VO2) before and shortly after two-thirds hepatectomy or sham operation at thermoneutrality (28 °C), and again after administration of propranolol (5 mg/kg). The difference in RMR between the resting period and propranolol treated period was used to represent the DIT. Their result suggests that liver is the major (70–100%) effector of the DIT [39][40]. In addition, Wallace et al. have demonstrated for the first time that the enhancement of specific calorigenic metabolic processes such as mitochondrial glycerophosphate oxidase within the liver contributes significantly to the heat production of DIT in cafeteria-fed rats [41]. These observations implicate that hepatic tissue might substantially take part in DIT under postprandial conditions.

6. Leptin

The adipocyte-derived leptin is a key factor in the regulation of energy balance [42], which is significantly increased in the obese state [43]. In fact, leptin has been reported to activate BAT sympathetic activity [44] and heat production [45][46][47]. In addition, a recent report has shown that refeeding increased plasma leptin concentrations in 48-h-fasted lean rats and leptin could mediate the increases in body temperature through hypothalamus-adrenal medulla-adipose tissue crosstalk after a meal [48]. Accordingly, chronic leptin treatment could stimulate BAT-mediated thermogenesis in leptin-deficient ob/ob mice by enhancing sympathetic innervation and activation [49]. Furthermore, BAT-ectomized rats reduced the thermogenic effect of food by 60% [48], suggesting that BAT appears to be a crucial mediator of leptin-induced thermogenesis. However, some earlier studies have found that female leptin-deficient ob/ob mice fed a palatable cafeteria diet still result in increased leptin-independent SNS activity and thermogenesis in BAT [50]. Some other reports also pointed out that leptin do not possess thermogenic function [51][52] and act as the mediator of DIT. These controversial observations might attribute to the differences in gender, methods, and experimental condition, which are needed to be further elucidated.
In contrast to leptin, adiponectin exhibits several characteristics of inhibiting energy expenditure. For instance, adiponectin inhibits UCP1 expression by reducing ADRB3 expression in brown adipocytes, along with reducing BAT thermogenesis in mice [53]. Previous report showed that neither fasting nor refeeding changed adiponectin serum levels in both young and old male rats [54]. The involvement of adiponectin in DIT process remains ambiguous.

7. Muscle

Sarcolipin (SLN) is a regulator of the Sarco/endoplasmic reticulum Ca2+-ATPase (SERCA) pump in muscle has been proposed to play an important role in DIT [55][56][57][58] and EE [59]. For instance, SLN regulates muscle-based non-shivering thermogenesis and is up-regulated with HFD. In addition, SLN KO mice are prone to develop diet-induced obesity and glucose intolerance. On the other hand, mice with SLN gene deletion gained comparable weight as UCP1-deficient mice on HFD, implicating that loss of muscle-based thermogenesis has similar consequences on weight gain as loss of UCP1-mediated thermogenesis [57]. Moreover, the body weight of mice with SLN overexpression is significantly lower than that of littermate control and they were resistant to HFD-induced obesity [58]. These mechanistic experiments indicated that SLN as an uncoupler of SERCA pump might create both energy demand and increase energy expenditure and are essential for counter-regulation of diet-induced energy intake.

8. Thyroid Hormones

Thyroid hormones, thyroxine (T4) and triiodothyronine (T3), have been well-documented to be a crucial determinant of energy expenditure and basal metabolic rate and also involved in the regulation of thermogenic responses to cold and diet [60]. Both cold-challenged and cafeteria-fed rats exhibited increases in circulating thyroid hormone levels [61]. In rats, overnutrition induced by a cafeteria diet is accompanied by a large increase in EE along with plasma T3 concentration [62]. T3 also acts as the main regulator of producing DIT in birds [63]. Accordingly, long-term over-feeding in men also exhibited accelerated metabolic rate and an increase in circulating T3 level [64]. Taken together, these observations implicate that thyroid hormone, especially T3, might substantially contribute to the generation of DIT under postprandial condition.


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