Thermogenesis and metabolic homeostasis work hand in hand, thanks to BAT’s proper function. Indeed, BAT can metabolize nutrients, such as glucose and fatty acids, and convert them into heat instead of ATP. This mechanism is called non-shivering thermogenesis, and it is made possible by mitochondrial uncoupling protein 1 (UCP-1). Furthermore, proper mitochondrial function and quality are essential for the BAT metabolic and thermogenic processes. Therefore, maintaining mitochondrial homeostasis is crucial for BAT’s metabolic maintenance.
Brown adipose tissue (BAT) is a specialized adipocyte group that converts nutrients, like glucose and fatty acids, into heat. Indeed, this thermogenic process is possible due to the high mitochondrial concentration and uncoupling protein 1 (UCP1).
Furthermore, this thermogenic mechanism is essential to maintain core body temperature and survival when exposed to cold temperatures. Indeed, when exposed to cold weather, brown adipocyte’s mitochondria convert nutrients into protons and stores them in the mitochondrial inner membrane. Consequently, these stored protons are converted into heat by uncoupling protein 1 (UCP1)-mediated proton leak. Lastly, the heat produced by UCP1 is by the blood flow to maintain body temperature. This mechanism is called non-shivering thermogenesis, and it promotes metabolic homeostasis by modulating energy expenditure.
This activation pathway shows that mitochondrial function and quality are essential for thermoregulation and metabolic homeostasis. Furthermore, this positions mitochondrial health in the central stage of human survival mechanisms and energy production. In addition, as mitochondrial integrity becomes paramount for proper BAT function, their biogenesis, repair, and removal are critical for human health.
Recent studies have focused on increasing BAT by several mechanisms that have proven to improve mitochondrial function. Furthermore, these studies challenged brown adipocytes from mice with cold temperatures to observe mitochondrial behavior and, most important, quality control.
In the first study, the researchers observed the mitochondrial ultrastructure of mice by electron microscopic (EM) images. Afterward, the mice were divided into two groups; the first was subjected to 4 °C (cold-challenge) vs. 30 °C (thermoneuturality) for seven days.
Furthermore, the EM images reported an increased presence of mitophagosomes in cold-challenged mouse BAT. Also, there was an increased expression of mRNA of mammalian autophagic membrane markers microtubule-associated protein light chain 3 (Map1lc3a) and ubiquitin-interacting protein p62 (Sqstm1). Consequently, these findings coincided with an increased concentration of UCP1, cytochrome c oxidase 1 (mt-Co1), cytochrome c oxidase II (mt-Co2), and ATP-synthase 6 (mt-Atp6). All of these results point to the fact that cold exposure increases mitophagy, which improves mitochondrial quality. Also, this shows that cold exposure increases UCP1 and cytochrome concentration, which can increase BAT’s size and total metabolic capacity.
The second study focused on the interaction of BAT’s mitochondrial and endoplasmic reticulum (ER) health. Indeed, this study reports how BAT adaptive recruitment process during cold adaptation interacts with ER’s protein and lipid synthesis. Furthermore, they also discuss the importance of a high-fat diet consumption and how this excess nutrient consumption might lead to the whitening of this tissue and reduced metabolic capacity.
ER’s cellular function is to synthesize proteins and lipids, and by doing so, this creates metabolic homeostasis. In addition, ER has its maintenance mechanism mediated by the unfolded protein response (UPR). Indeed, UPR is a molecular network that promotes enhanced protein capacity and reduces protein translation and ER-associated protein degradation (ERAD) of damaged proteins through the ubiquitin-proteosome system (UPS). This system is inhibited in obese patient’s livers, which leads to inflammatory stress pathways. Furthermore, as ER concentration is low in brown adipocytes leads to believe that this pathway is dispensable or that brown adipocytes need an alternative protective pathway.
This study confirmed that the ER-localized transcription factor nuclear factor erythroid-2, like-1 (Nfe2l1, also known as Nrf1), was a critical driver of this quality control system. Also, the cold-induced activation of the Nrf1 pathway increased proteasomal activity, maintained ER homeostasis, thermoregulation, and cellular integrity.
Conditions complex as obesity or an injury have something in common with survival: mitochondrial integrity. As the studies on mitochondrial show their different metabolic or thermoregulatory functions, we notice that they run the show. In Functional Medicine, we seek to treat the root cause of health issues, supplying the right amount of vitamins and minerals to increase mitochondrial function or integrity. Most of the time, this means that we need to restore gut health and fix macro and micronutrient depletion, ultimately leading to restoring membrane function. This has a domino effect that results in fast injury recovery, less pain, inflammation reduction, and wellbeing. – Ana Paola Rodríguez Arciniega, MS
Bartelt, Alexander et al. “Brown adipose tissue thermogenic adaptation require Nrf1-mediated proteasomal activity.” Nature medicine vol. 24,3 (2018): 292-303. doi:10.1038/nm.4481
Lu, Yuan et al. “Mitophagy is required for brown adipose tissue mitochondrial homeostasis during cold challenge.” Scientific Reports vol. 8,1 8251. 29 May. 2018, doi:10.1038/s41598-018-26394-5
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