Publications by authors named "Dina Laznik-Bogoslavski"

Uptake of circulating succinate by brown adipose tissue (BAT) and beige fat elevates whole-body energy expenditure, counteracts obesity and antagonizes systemic tissue inflammation in mice. The plasma membrane transporters that facilitate succinate uptake in these adipocytes remain undefined. Here we elucidate a mechanism underlying succinate import into BAT via monocarboxylate transporters (MCTs).

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Article Synopsis
  • Researchers studied brown fat tissue (BAT) in a diverse group of 163 mice to learn how it affects metabolism, unlike past studies which focused on just one type of mouse.
  • They found over 10,000 proteins in BAT and figured out how some work together, identifying 2,578 proteins that help regulate BAT.
  • The team also discovered specific proteins like SFXN5, LETMD1, and ATP1A2 that can help control fat burning and body fat, helping us understand more about how BAT works in metabolism.
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  • Uncoupling protein 1 (UCP1) is crucial for regulating energy expenditure in brown and beige fat, but previous loss-of-function models showed issues with the entire energy pathway, making UCP1's role unclear.
  • Researchers identified a specific site (cysteine-253) on UCP1 that, when modified, boosts its activity and created a genetic mouse model lacking this site (UCP1 C253A) to study its effects.
  • UCP1 C253A mice had reduced thermogenesis but did not gain extra fat; instead, they experienced tissue stress and inflammation in males, which was mitigated in females due to higher systemic estrogen levels.
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In response to skeletal muscle contraction during exercise, paracrine factors coordinate tissue remodeling, which underlies this healthy adaptation. Here we describe a pH-sensing metabolite signal that initiates muscle remodeling upon exercise. In mice and humans, exercising skeletal muscle releases the mitochondrial metabolite succinate into the local interstitium and circulation.

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  • Oxidation of cysteine thiols by reactive oxygen species (ROS) activates thermogenesis in brown and beige fat tissues, crucial for energy expenditure.
  • The study developed a mass spectrometric method to detect selenium incorporation into proteins, uncovering unexpected selenium use in proteins not conventionally coded for it.
  • Increased cellular levels of organic selenium, particularly through dietary supplementation, enhanced selenium incorporation into the uncoupling protein 1 (UCP1), boosting energy expenditure and offering protection against obesity.
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The peroxisome-proliferator receptor-γ (PPARγ) is expressed in multiple cancer types. Recently, our group has shown that PPARγ is phosphorylated on serine 273 (S273), which selectively modulates the transcriptional program controlled by this protein. PPARγ ligands, including thiazolidinediones (TZDs), block S273 phosphorylation.

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Diet-induced thermogenesis is an important homeostatic mechanism that limits weight gain in response to caloric excess and contributes to the relative stability of body weight in most individuals. We previously demonstrated that creatine enhances energy expenditure through stimulation of mitochondrial ATP turnover, but the physiological role and importance of creatine energetics in adipose tissue have not been explored. Here, we have inactivated the first and rate-limiting enzyme of creatine biosynthesis, glycine amidinotransferase (GATM), selectively in fat (Adipo-Gatm KO).

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Brown and beige adipose tissues can dissipate chemical energy as heat through thermogenic respiration, which requires uncoupling protein 1 (UCP1). Thermogenesis from these adipocytes can combat obesity and diabetes, encouraging investigation of factors that control UCP1-dependent respiration in vivo. Here we show that acutely activated thermogenesis in brown adipose tissue is defined by a substantial increase in levels of mitochondrial reactive oxygen species (ROS).

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Thermogenic brown and beige adipose tissues dissipate chemical energy as heat, and their thermogenic activities can combat obesity and diabetes. Herein the functional adaptations to cold of brown and beige adipose depots are examined using quantitative mitochondrial proteomics. We identify arginine/creatine metabolism as a beige adipose signature and demonstrate that creatine enhances respiration in beige-fat mitochondria when ADP is limiting.

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Obesity-linked insulin resistance is a major precursor to the development of type 2 diabetes. Previous work has shown that phosphorylation of PPARγ (peroxisome proliferator-activated receptor γ) at serine 273 by cyclin-dependent kinase 5 (Cdk5) stimulates diabetogenic gene expression in adipose tissues. Inhibition of this modification is a key therapeutic mechanism for anti-diabetic drugs that bind PPARγ, such as the thiazolidinediones and PPARγ partial agonists or non-agonists.

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Diabetes risk increases significantly with age and correlates with lower oxidative capacity in muscle. Decreased expression of peroxisome proliferator-activated receptor-γ coactivator-1α (Pgc-1α) and target gene pathways involved in mitochondrial oxidative phosphorylation are associated with muscle insulin resistance, but a causative role has not been established. We sought to determine whether a decline in Pgc-1α and oxidative gene expression occurs during aging and potentiates the development of age-associated insulin resistance.

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Exercise can improve cognitive function and has been linked to the increased expression of brain-derived neurotrophic factor (BDNF). However, the underlying molecular mechanisms driving the elevation of this neurotrophin remain unknown. Here we show that FNDC5, a previously identified muscle protein that is induced in exercise and is cleaved and secreted as irisin, is also elevated by endurance exercise in the hippocampus of mice.

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