
근육 불활성화는 골격근의 열 생성을 억제하고 갈색 지방 조직의 열 생성을 보상적으로 활성화시킨다. 갈색 지방 조직은 골격근에서 유래된 분지 사슬 아미노산을 에너지 기질로 이용하며, 골격근에서 방출된 인터루킨-6가 근육의 분지 사슬 아미노산 생산을 자극하여 갈색 지방 조직의 열 생성을 지원한다.


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Endotherms increase the rate of metabolism in metabolic organs as one strategy to cope with a decline in temperature of the external environment. However, an additional major contributor to maintenance of body temperature in a cold environment is contraction-based thermogenesis in skeletal muscle. Here we show that impairment of hind limb muscle contraction by cast immobilization suppresses skeletal muscle thermogenesis and activates brown adipose tissue (BAT) thermogenesis as a compensatory mechanism. BAT utilizes free branched-chain amino acids (BCAAs) derived from skeletal muscle as an energy substrate for thermogenesis, and interleukin-6 released by skeletal muscle stimulates BCAA production in muscle for support of BAT thermogenesis. Our findings suggest that BAT and skeletal muscle cooperate to maintain body temperature in endotherms.

### Competing Interest Statement

The authors have declared no competing interest.

Brown Adipose Tissue and Skeletal Muscle Coordinately Contribute to Thermogenesis in Mice

근육-불활성화가-갈색-지방-조직과-골격근의-열-생성에-미치는-영향


근육 불활성화가 갈색 지방 조직과 골격근의 열 생성에 미치는 영향


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SLC35G1은 장상피세포의 기저측막에 위치하여 구연산 배출에 관여하는 고염화물 감수성 수송체이다.


The intestinal absorption of essential nutrients, especially those not readily biosynthesized, is a critical physiological process for maintaining homeostasis. Numerous studies have indicated that intestinal absorption is mediated by various membrane transporters. Citrate, a crucial bioactive compound produced as an intermediate in the Krebs cycle, is absorbed in the small intestine through carrier-mediated systems because of its high hydrophilicity. While the luminal absorption of citrate is mediated by Na+-dicarboxylate cotransporter 1 (NaDC1), the mechanism governing the release of the transported citrate into the bloodstream remains unknown. Here, we explored the transporters responsible for intestinal citrate absorption at the basolateral membrane, focusing on highly expressed orphan transporters in the small intestine as candidates. Consequently, SLC35G1, originally identified as a partner of stromal interaction molecule 1, a cell surface transmembrane glycoprotein, was found to play a role in the intestinal absorption of citrate at the basolateral membrane. Furthermore, our results revealed that SLC35G1-mediated citrate transport was diminished by chloride ions at extracellular concentrations. This suggests that SLC35G1, to our best knowledge, is the first transporter identified to be extremely sensitive to chloride ions among those functioning on the basolateral membrane of intestinal epithelial cells. This study provides valuable insights into the intestinal absorption of citrate and significantly contributes to elucidating the poorly understood molecular basis of the intestinal absorption system.

### Competing Interest Statement

The authors have declared no competing interest.

SLC35G1: A highly chloride-sensitive transporter responsible for the basolateral membrane transport in intestinal citrate absorption

장내-구연산-흡수에-관여하는-고염화물-감수성-수송체-slc35g1


장내 구연산 흡수에 관여하는 고염화물 감수성 수송체 SLC35G1



TRPV4는 ANO1과의 상호작용을 통해 온도 의존적 발한에 관여한다.


Reports indicate that an interaction between TRPV4 and anoctamin 1 could be widely involved in water efflux of exocrine glands, suggesting that the interaction could play a role in perspiration. In secretory cells of sweat glands present in mouse foot pads, TRPV4 clearly colocalized with cytokeratin 8, anoctamin 1 (ANO1) and aquaporin-5 (AQP5). Mouse sweat glands showed TRPV4-dependent cytosolic Ca2+ increases that was inhibited by menthol. Acetylcholine-stimulated sweating in foot pads was temperature-dependent in wild-type, but not in TRPV4-deficient mice, and was inhibited by menthol both in wild-type and TRPM8KO mice. The basal sweating without acetylcholine stimulation was inhibited by an ANO1 inhibitor. Sweating could be important for maintaining friction forces in mouse foot pads, and this possibility is supported by the finding that wild-type mice climbed up a slippery slope more easily than TRPV4-deleted mice. Furthermore, TRPV4 expression was significantly higher in controls and normohidrotic skin from patients with AIGA (acquired idiopathic generalized anhidrosis) compared to anhidrotic skin from patients with AIGA. Collectively, TRPV4 is likely involved in temperature-dependent perspiration via interactions with ANO1, and TRPV4 itself or the TRPV4/ANO 1 complex would be targets to develop agents that regulate perspiration.

### Competing Interest Statement

The authors have declared no competing interest.

Involvement of TRPV4 in temperature-dependent perspiration in mice

마우스에서-trpv4가-온도-의존적-발한에-관여한다


마우스에서 TRPV4가 온도 의존적 발한에 관여한다



명시적 및 암시적 선행 지식을 결합하여 rPPG 작업의 일반화 성능 향상


rppg의-일반화된-원격-생리-측정을-위한-명시적-및-암시적-선행-지식-통합을-통한-진보


rPPG의 일반화된 원격 생리 측정을 위한 명시적 및 암시적 선행 지식 통합을 통한 진보
