Lipid Droplets: A Cellular Organelle Vital for Thermogenesis

Chen, Lupeng; Jin, Y.; Wu, Jian; Ren, Zhuqing

doi:10.7150/ijbs.77051

Cited by 14 publications

(4 citation statements)

References 107 publications

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“…This thermogenic response is orchestrated by UCP-1, which is prevalent in the mitochondrial membrane of brown fat cells and disrupts the typical pathway of oxidative phosphorylation. [5] In this study, we observed a decrease in the lipid area within BAT when the mice were housed at low temperatures (22°C and 14°C) (Supplementary Fig. 4A and 4B), Furthermore, Western blot analysis con rmed that cold temperature housing conditions activate lipolysis (Supplementary Fig.…”

Section: Alterations In Lipid Composition Within Thermogenic Adipose ...supporting

confidence: 50%

Brown fat-specific mitoribosomal function is crucial for preventing cold exposure-induced bone loss

Tian,

Moon,

Nga

et al. 2024

Preprint

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This study investigates the relationship between ambient temperature, brown adipose tissue (BAT) function, and bone metabolism, revealing how cold exposure and BAT mitochondrial activity influence bone health. Utilizing ovariectomized (OVX) mice to model primary osteoporosis and BAT-specific mitochondrial dysfunction (BKO) mice, we explored the effects of housing temperature on bone density, immune modulation in bone marrow, and the protective role of BAT against bone loss. The results showed that cold exposure universally decreases bone mass, increases osteoclastogenesis, and shifts bone marrow T-cell populations, suggesting a key role of the immune system in bone remodeling under cold stress. Crucially, the thermogenic function of BAT, underpinned by mitochondrial oxidative phosphorylation, protected against bone loss. Impairments in BAT function, either through surgical removal or mitochondrial dysfunction, exacerbated bone loss in cold environments, highlighting the importance of BAT metabolic activity for bone health. Additionally, we found that cold-induced alterations in BAT function led to systemic metabolic changes, including increased long-chain fatty acid levels, which directly and indirectly affected osteoclast differentiation and activity. These findings point to a systemic mechanism via which environmental temperature and BAT metabolism are interconnected with bone physiology, offering new insights into the metabolic and environmental determinants of bone health. In summary, our study underscores the complex interactions between ambient temperature, BAT function, and bone health, suggesting that novel bone disease therapies could be developed by targeting metabolic and environmental factors. Further research in these pathways may provide innovative approaches for managing bone health amid changing environmental conditions and metabolic dysfunctions.

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Section: Alterations In Lipid Composition Within Thermogenic Adipose ...supporting

confidence: 50%

Brown fat-specific mitoribosomal function is crucial for preventing cold exposure-induced bone loss

Tian,

Moon,

Nga

et al. 2024

Preprint

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“…Obesity is universally considered to be a metabolic problem caused by the unnecessary and dangerous excessive accumulation of fat deposits (mostly TAG) in specialized cells, adipocytes [737], as well as in a large number of micro-droplets present mainly in the cell cytoplasm of several tissues and organs, such as the muscle [738,739] or liver [740,741]. Cell lipid droplets play important functions in the rapid availability of TAG for energy, defense [742,743], thermogenesis [744], and as short-term (or processing) energy buffers [745,746]. In adipocytes, lipid droplets play an important role in the transport of TAG and in their coalescence into the large storage vacuoles [747,748].…”

Section: The Adipose Organ An Energy-handling Specialization Of the Ctmentioning

confidence: 99%

The Metabolic Syndrome, a Human Disease

Alemany

2024

IJMS

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This review focuses on the question of metabolic syndrome (MS) being a complex, but essentially monophyletic, galaxy of associated diseases/disorders, or just a syndrome of related but rather independent pathologies. The human nature of MS (its exceptionality in Nature and its close interdependence with human action and evolution) is presented and discussed. The text also describes the close interdependence of its components, with special emphasis on the description of their interrelations (including their syndromic development and recruitment), as well as their consequences upon energy handling and partition. The main theories on MS’s origin and development are presented in relation to hepatic steatosis, type 2 diabetes, and obesity, but encompass most of the MS components described so far. The differential effects of sex and its biological consequences are considered under the light of human social needs and evolution, which are also directly related to MS epidemiology, severity, and relations with senescence. The triggering and maintenance factors of MS are discussed, with especial emphasis on inflammation, a complex process affecting different levels of organization and which is a critical element for MS development. Inflammation is also related to the operation of connective tissue (including the adipose organ) and the widely studied and acknowledged influence of diet. The role of diet composition, including the transcendence of the anaplerotic maintenance of the Krebs cycle from dietary amino acid supply (and its timing), is developed in the context of testosterone and β-estradiol control of the insulin-glycaemia hepatic core system of carbohydrate-triacylglycerol energy handling. The high probability of MS acting as a unique complex biological control system (essentially monophyletic) is presented, together with additional perspectives/considerations on the treatment of this ‘very’ human disease.

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“…White adipocytes represent the largest component of white adipose tissue and contain LDs, organelles that store TG, which have a "buffering" effect on the release of FAs. 95 TG require hydrolysis to liberate FAs and glycerol so that they can enter or leave adipocytes or else be transported across the cell membrane by means of specialized vesicles. 96 In humans, circulating TG are bound to water-soluble The hydrolysis of TG in adipocytes is catalyzed by lipases, in a process known as lipolysis.…”

Section: Tg Metabolism In Adipocytes Under Physiological Conditionsmentioning

confidence: 99%

Inflammation‐mediated metabolic regulation in adipose tissue

Xu,

Lu,

Gao

et al. 2024

Obesity Reviews

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SummaryChronic inflammation of adipose tissue is a prominent characteristic of many metabolic diseases. Lipid metabolism in adipose tissue is consistently dysregulated during inflammation, which is characterized by substantial infiltration by proinflammatory cells and high cytokine concentrations. Adipose tissue inflammation is caused by a variety of endogenous factors, such as mitochondrial dysfunction, reactive oxygen species (ROS) production, endoplasmic reticulum (ER) stress, cellular senescence, ceramides biosynthesis and mediators of lipopolysaccharides (LPS) signaling. Additionally, the gut microbiota also plays a crucial role in regulating adipose tissue inflammation. Essentially, adipose tissue inflammation arises from an imbalance in adipocyte metabolism and the regulation of immune cells. Specific inflammatory signals, including nuclear factor‐κB (NF‐κB) signaling, inflammasome signaling and inflammation‐mediated autophagy, have been shown to be involved in the metabolic regulation. The pathogenesis of metabolic diseases characterized by chronic inflammation (obesity, insulin resistance, atherosclerosis and nonalcoholic fatty liver disease [NAFLD]) and recent research regarding potential therapeutic targets for these conditions are also discussed in this review.

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Lipid Droplets: A Cellular Organelle Vital for Thermogenesis

Cited by 14 publications

References 107 publications

Brown fat-specific mitoribosomal function is crucial for preventing cold exposure-induced bone loss

Brown fat-specific mitoribosomal function is crucial for preventing cold exposure-induced bone loss

The Metabolic Syndrome, a Human Disease

Inflammation‐mediated metabolic regulation in adipose tissue

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