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Article ; Online: Small intestinal CaSR-dependent and CaSR-independent protein sensing regulates feeding and glucose tolerance in rats.

Li, Rosa J W / Barros, Daniel R / Kuah, Rachel / Lim, Yu-Mi / Gao, Anna / Beaudry, Jacqueline L / Zhang, Song-Yang / Lam, Tony K T

Nature metabolism

2024 Volume 6, Issue 1, Page(s) 39–49

Abstract: Proteins activate small intestinal calcium sensing receptor (CaSR) and/or peptide transporter 1 (PepT1) to increase hormone ... ...

Abstract	Proteins activate small intestinal calcium sensing receptor (CaSR) and/or peptide transporter 1 (PepT1) to increase hormone secretion
MeSH term(s)	Animals ; Male ; Rats ; Caseins/metabolism ; Gastrointestinal Hormones/metabolism ; Glucose/metabolism ; Intestine, Small/metabolism ; Receptors, Calcium-Sensing/metabolism
Chemical Substances	Caseins ; Gastrointestinal Hormones ; Glucose (IY9XDZ35W2) ; Receptors, Calcium-Sensing ; extracellular calcium cation-sensing receptor, rat
Language	English
Publishing date	2024-01-02
Publishing country	Germany
Document type	Journal Article
ISSN	2522-5812
ISSN (online)	2522-5812
DOI	10.1038/s42255-023-00942-4
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Article ; Online: Inhibition of Sodium-Glucose Cotransporter-2 during Serum Deprivation Increases Hepatic Gluconeogenesis via the AMPK/AKT/FOXO Signaling Pathway.

Lee, Jinmi / Hong, Seok-Woo / Kim, Min-Jeong / Lim, Yu-Mi / Moon, Sun Joon / Kwon, Hyemi / Park, Se Eun / Rhee, Eun-Jung / Lee, Won-Young

Endocrinology and metabolism (Seoul, Korea)

2024 Volume 39, Issue 1, Page(s) 98–108

Abstract: Backgruound: Sodium-dependent glucose cotransporter 2 (SGLT2) mediates glucose reabsorption in the renal proximal tubules, and SGLT2 inhibitors are used as therapeutic agents for treating type 2 diabetes mellitus. This study aimed to elucidate the ... ...

Abstract	Backgruound: Sodium-dependent glucose cotransporter 2 (SGLT2) mediates glucose reabsorption in the renal proximal tubules, and SGLT2 inhibitors are used as therapeutic agents for treating type 2 diabetes mellitus. This study aimed to elucidate the effects and mechanisms of SGLT2 inhibition on hepatic glucose metabolism in both serum deprivation and serum supplementation states. Methods: Huh7 cells were treated with the SGLT2 inhibitors empagliflozin and dapagliflozin to examine the effect of SGLT2 on hepatic glucose uptake. To examine the modulation of glucose metabolism by SGLT2 inhibition under serum deprivation and serum supplementation conditions, HepG2 cells were transfected with SGLT2 small interfering RNA (siRNA), cultured in serum-free Dulbecco's modified Eagle's medium for 16 hours, and then cultured in media supplemented with or without 10% fetal bovine serum for 8 hours. Results: SGLT2 inhibitors dose-dependently decreased hepatic glucose uptake. Serum deprivation increased the expression levels of the gluconeogenesis genes peroxisome proliferator-activated receptor gamma co-activator 1 alpha (PGC-1α), glucose 6-phosphatase (G6pase), and phosphoenolpyruvate carboxykinase (PEPCK), and their expression levels during serum deprivation were further increased in cells transfected with SGLT2 siRNA. SGLT2 inhibition by siRNA during serum deprivation induces nuclear localization of the transcription factor forkhead box class O 1 (FOXO1), decreases nuclear phosphorylated-AKT (p-AKT), and p-FOXO1 protein expression, and increases phosphorylated-adenosine monophosphate-activated protein kinase (p-AMPK) protein expression. However, treatment with the AMPK inhibitor, compound C, reversed the reduction in the protein expression levels of nuclear p- AKT and p-FOXO1 and decreased the protein expression levels of p-AMPK and PEPCK in cells transfected with SGLT2 siRNA during serum deprivation. Conclusion: These data show that SGLT2 mediates glucose uptake in hepatocytes and that SGLT2 inhibition during serum deprivation increases gluconeogenesis via the AMPK/AKT/FOXO1 signaling pathway.
MeSH term(s)	Humans ; AMP-Activated Protein Kinases/metabolism ; Diabetes Mellitus, Type 2/drug therapy ; Gluconeogenesis/genetics ; Glucose ; Phosphoenolpyruvate Carboxykinase (ATP)/genetics ; Phosphoenolpyruvate Carboxykinase (ATP)/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Proto-Oncogene Proteins c-akt/pharmacology ; Proto-Oncogene Proteins c-akt/therapeutic use ; RNA, Small Interfering/genetics ; RNA, Small Interfering/metabolism ; RNA, Small Interfering/pharmacology ; Signal Transduction ; Sodium/metabolism ; Sodium/pharmacology ; Sodium/therapeutic use ; Sodium-Glucose Transporter 2/metabolism ; Sodium-Glucose Transporter 2/pharmacology ; Sodium-Glucose Transporter 2/therapeutic use ; Sodium-Glucose Transporter 2 Inhibitors/pharmacology ; Sodium-Glucose Transporter 2 Inhibitors/therapeutic use
Chemical Substances	AMP-Activated Protein Kinases (EC 2.7.11.31) ; Glucose (IY9XDZ35W2) ; Phosphoenolpyruvate Carboxykinase (ATP) (EC 4.1.1.49) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; RNA, Small Interfering ; Sodium (9NEZ333N27) ; Sodium-Glucose Transporter 2 ; Sodium-Glucose Transporter 2 Inhibitors ; SLC5A2 protein, human
Language	English
Publishing date	2024-01-03
Publishing country	Korea (South)
Document type	Journal Article
ZDB-ID	2802452-7
ISSN	2093-5978 ; 2093-5978
ISSN (online)	2093-5978
ISSN	2093-5978
DOI	10.3803/EnM.2023.1786
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Article ; Online: The Role of Autophagy in Systemic Metabolism and Human-Type Diabetes.

Kim, Jinyoung / Lim, Yu-Mi / Lee, Myung-Shik

Molecules and cells

2018 Volume 41, Issue 1, Page(s) 11–17

Abstract: Autophagy is critical for the maintenance of organelle function and intracellular nutrient environment. Autophagy is also involved in systemic metabolic homeostasis, and its dysregulation can lead to or accelerate the development of metabolic disorders. ... ...

Abstract	Autophagy is critical for the maintenance of organelle function and intracellular nutrient environment. Autophagy is also involved in systemic metabolic homeostasis, and its dysregulation can lead to or accelerate the development of metabolic disorders. While the role of autophagy in the global metabolism of model organisms has been investigated mostly using site-specific genetic knockout technology, the impact of dysregulated autophagy on systemic metabolism has been unclear. Here, we review recent papers showing the role of autophagy in systemic metabolism and in the development of metabolic disorders. Also included are data suggesting the role of autophagy in human-type diabetes, which are different in several key aspects from murine models of diabetes. The results shown here support the view that autophagy modulation could be a new modality for the treatment of metabolic syndrome associated with lipid overload and human-type diabetes.
MeSH term(s)	Autophagy/physiology ; Diabetes Mellitus/physiopathology ; Energy Metabolism/physiology ; Homeostasis/physiology ; Humans ; Inflammation/physiopathology ; Insulin Resistance/physiology ; Metabolic Diseases/physiopathology ; Models, Biological ; Obesity/physiopathology
Language	English
Publishing date	2018-01-23
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1148964-9
ISSN	0219-1032 ; 1016-8478
ISSN (online)	0219-1032
ISSN	1016-8478
DOI	10.14348/molcells.2018.2228
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Article ; Online: Small intestinal taurochenodeoxycholic acid-FXR axis alters local nutrient-sensing glucoregulatory pathways in rats.

Waise, T M Zaved / Lim, Yu-Mi / Danaei, Zahra / Zhang, Song-Yang / Lam, Tony K T

Molecular metabolism

2020 Volume 44, Page(s) 101132

Abstract: Objective: The mechanism of nutrient sensing in the upper small intestine (USI) and ileum that regulates glucose homeostasis remains elusive. Short-term high-fat (HF) feeding increases taurochenodeoxycholic acid (TCDCA; an agonist of farnesoid X ... ...

Abstract	Objective: The mechanism of nutrient sensing in the upper small intestine (USI) and ileum that regulates glucose homeostasis remains elusive. Short-term high-fat (HF) feeding increases taurochenodeoxycholic acid (TCDCA; an agonist of farnesoid X receptor (FXR)) in the USI and ileum of rats, and the increase of TCDCA is prevented by transplantation of microbiota obtained from the USI of healthy donors into the USI of HF rats. However, whether changes of TCDCA-FXR axis in the USI and ileum alter nutrient sensing remains unknown. Methods: Intravenous glucose tolerance test was performed in rats that received USI or ileal infusion of nutrients (i.e., oleic acids or glucose) via catheters placed toward the lumen of USI and/or ileum, while mechanistic gain- and loss-of-function studies targeting the TCDCA-FXR axis or bile salt hydrolase activity in USI and ileum were performed. Results: USI or ileum infusion of nutrients increased glucose tolerance in healthy but not HF rats. Transplantation of healthy microbiome obtained from USI into the USI of HF rats restored nutrient sensing and inhibited FXR via a reduction of TCDCA in the USI and ileum. Further, inhibition of USI and ileal FXR enhanced nutrient sensing in HF rats, while inhibiting USI (but not ileal) bile salt hydrolase of HF rats transplanted with healthy microbiome activated FXR and disrupted nutrient sensing in the USI and ileum. Conclusions: We reveal a TCDCA-FXR axis in both the USI and ileum that is necessary for the upper small intestinal microbiome to govern local nutrient-sensing glucoregulatory pathways in rats.
MeSH term(s)	Animals ; Bile Acids and Salts ; Gastrointestinal Microbiome ; Glucose/metabolism ; Glucose Tolerance Test ; Homeostasis ; Ileum/metabolism ; Intestine, Small/metabolism ; Male ; Nutrients ; Rats ; Rats, Sprague-Dawley ; Taurochenodeoxycholic Acid/metabolism
Chemical Substances	Bile Acids and Salts ; Taurochenodeoxycholic Acid (516-35-8) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2020-11-29
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2708735-9
ISSN	2212-8778 ; 2212-8778
ISSN (online)	2212-8778
ISSN	2212-8778
DOI	10.1016/j.molmet.2020.101132
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Article ; Online: Metformin triggers a kidney GDF15-dependent area postrema axis to regulate food intake and body weight.

Zhang, Song-Yang / Bruce, Kyla / Danaei, Zahra / Li, Rosa J W / Barros, Daniel R / Kuah, Rachel / Lim, Yu-Mi / Mariani, Laura H / Cherney, David Z / Chiu, Jennifer F M / Reich, Heather N / Lam, Tony K T

Cell metabolism

2023 Volume 35, Issue 5, Page(s) 875–886.e5

Abstract: Metformin, the most widely prescribed medication for obesity-associated type 2 diabetes (T2D), lowers plasma glucose levels, food intake, and body weight in rodents and humans, but the mechanistic site(s) of action remain elusive. Metformin increases ... ...

Abstract	Metformin, the most widely prescribed medication for obesity-associated type 2 diabetes (T2D), lowers plasma glucose levels, food intake, and body weight in rodents and humans, but the mechanistic site(s) of action remain elusive. Metformin increases plasma growth/differentiation factor 15 (GDF15) levels to regulate energy balance, while GDF15 administration activates GDNF family receptor α-like (GFRAL) that is highly expressed in the area postrema (AP) and the nucleus of the solitary tract (NTS) of the hindbrain to lower food intake and body weight. However, the tissue-specific contribution of plasma GDF15 levels after metformin treatment is still under debate. Here, we found that metformin increased plasma GDF15 levels in high-fat (HF) fed male rats through the upregulation of GDF15 synthesis in the kidney. Importantly, the kidney-specific knockdown of GDF15 expression as well as the AP-specific knockdown of GFRAL expression negated the ability of metformin to lower food intake and body weight gain. Taken together, we unveil the kidney as a target of metformin to regulate energy homeostasis through a kidney GDF15-dependent AP axis.
MeSH term(s)	Humans ; Male ; Rats ; Animals ; Metformin/pharmacology ; Area Postrema/metabolism ; Weight Loss ; Diabetes Mellitus, Type 2/metabolism ; Body Weight/physiology ; Eating ; Kidney/metabolism ; Growth Differentiation Factor 15/metabolism
Chemical Substances	Metformin (9100L32L2N) ; GDF15 protein, human ; Growth Differentiation Factor 15
Language	English
Publishing date	2023-04-14
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2176834-1
ISSN	1932-7420 ; 1550-4131
ISSN (online)	1932-7420
ISSN	1550-4131
DOI	10.1016/j.cmet.2023.03.014
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Article ; Online: Bioconverted Fruit Extract of Akebia Quinata Exhibits Anti-Obesity Effects in High-Fat Diet-Induced Obese Rats.

Lee, Seul Gi / Lee, Eunbi / Chae, Jongbeom / Kim, Jin Soo / Lee, Han-Saem / Lim, Yu-Mi / So, Jai-Hyun / Hahn, Dongyup / Nam, Ju-Ock

Nutrients

2022 Volume 14, Issue 21

Abstract: Akebia quinata, commonly called chocolate vine, has various bioactivities, including antioxidant and anti-obesity properties. However, the anti-obesity effects of bioconverted extracts of A. quinate have not been examined. In this study, A. quinata fruit ...

Abstract	Akebia quinata, commonly called chocolate vine, has various bioactivities, including antioxidant and anti-obesity properties. However, the anti-obesity effects of bioconverted extracts of A. quinate have not been examined. In this study, A. quinata fruit extracts was bioconverted using the enzyme isolated from the soybean paste fungi Aspergillus kawachii. To determine whether the bioconversion process could influence the anti-obesity effects of A. quinata fruit extracts, we employed 3T3-L1 adipocytes and HFD-induced obese rats. We observed that the bioconverted fruit extract of A. quinata (BFE) afforded anti-obesity effects, which were stronger than that for the non-bioconverted fruit extract (FE) of A. quinata. In 3T3-L1 adipocytes, treatment with BFE at concentrations of 20 and 40 μg reduced intracellular lipids by 74.8 (p < 0.05) and 54.9% (p < 0.01), respectively, without inducing cytotoxicity in preadipocytes. Moreover, the oral administration of BFE at the concentration of 300 mg/kg/day significantly reduced body and adipose tissue weights (p < 0.01) in HFD-induced obese rats. Plasma cholesterol values were reduced, whereas HDL was increased in BFE receiving rats. Although FE could exert anti-obesity effects, BFE supplementation induced more robust effects than FE. These results could be attributed to the bioconversion-induced alteration of bioactive compound content within the extract.
MeSH term(s)	Mice ; Rats ; Animals ; Diet, High-Fat/adverse effects ; Anti-Obesity Agents/pharmacology ; Adipogenesis ; Fruit ; 3T3-L1 Cells ; Obesity/drug therapy ; Obesity/etiology ; Plant Extracts/pharmacology ; Mice, Inbred C57BL
Chemical Substances	Anti-Obesity Agents ; Plant Extracts
Language	English
Publishing date	2022-11-05
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2518386-2
ISSN	2072-6643 ; 2072-6643
ISSN (online)	2072-6643
ISSN	2072-6643
DOI	10.3390/nu14214683
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Article ; Online: FXR in the dorsal vagal complex is sufficient and necessary for upper small intestinal microbiome-mediated changes of TCDCA to alter insulin action in rats.

Zhang, Song-Yang / Li, Rosa J W / Lim, Yu-Mi / Batchuluun, Battsetseg / Liu, Huiying / Waise, T M Zaved / Lam, Tony K T

Gut

2020 Volume 70, Issue 9, Page(s) 1675–1683

Abstract: Objective: Conjugated bile acids are metabolised by upper small intestinal microbiota, and serum levels of taurine-conjugated bile acids are elevated and correlated with insulin resistance in people with type 2 diabetes. However, whether changes in ... ...

Abstract	Objective: Conjugated bile acids are metabolised by upper small intestinal microbiota, and serum levels of taurine-conjugated bile acids are elevated and correlated with insulin resistance in people with type 2 diabetes. However, whether changes in taurine-conjugated bile acids are necessary for small intestinal microbiome to alter insulin action remain unknown. Design: We evaluated circulating and specifically brain insulin action using the pancreatic-euglycaemic clamps in high-fat (HF) versus chow fed rats with or without upper small intestinal healthy microbiome transplant. Chemical and molecular gain/loss-of-function experiments targeting specific taurine-conjugated bile acid-induced changes of farnesoid X receptor (FXR) in the brain were performed in parallel. Results: We found that short-term HF feeding increased the levels of taurochenodeoxycholic acid (TCDCA, an FXR ligand) in the upper small intestine, ileum, plasma and dorsal vagal complex (DVC) of the brain. Transplantation of upper small intestinal healthy microbiome into the upper small intestine of HF rats not only reversed the rise of TCDCA in all reported tissues but also enhanced the ability of either circulating hyperinsulinaemia or DVC insulin action to lower glucose production. Further, DVC infusion of TCDCA or FXR agonist negated the enhancement of insulin action, while genetic knockdown or chemical inhibition of FXR in the DVC of HF rats reversed insulin resistance. Conclusion: Our findings indicate that FXR in the DVC is sufficient and necessary for upper small intestinal microbiome-mediated changes of TCDCA to alter insulin action in rats, and highlight a previously unappreciated TCDCA-FXR axis linking gut microbiome and host insulin action.
MeSH term(s)	Animals ; Brain/metabolism ; Brain Chemistry ; Brain Stem/metabolism ; Brain Stem/physiology ; Diet, High-Fat ; Fecal Microbiota Transplantation ; Gastrointestinal Microbiome/physiology ; Gene Knockdown Techniques ; Glucose Clamp Technique ; Insulin Resistance/physiology ; Intestine, Small/metabolism ; Intestine, Small/microbiology ; Rats ; Receptors, Cytoplasmic and Nuclear/analysis ; Receptors, Cytoplasmic and Nuclear/metabolism ; Taurochenodeoxycholic Acid/analysis ; Taurochenodeoxycholic Acid/metabolism
Chemical Substances	Receptors, Cytoplasmic and Nuclear ; farnesoid X-activated receptor (0C5V0MRU6P) ; Taurochenodeoxycholic Acid (516-35-8)
Language	English
Publishing date	2020-10-21
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80128-8
ISSN	1468-3288 ; 0017-5749
ISSN (online)	1468-3288
ISSN	0017-5749
DOI	10.1136/gutjnl-2020-321757
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Zs.A 160: Show issues

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Article ; Online: Nutrient infusion in the dorsal vagal complex controls hepatic lipid and glucose metabolism in rats.

Li, Rosa J W / Batchuluun, Battsetseg / Zhang, Song-Yang / Abraham, Mona A / Wang, Beini / Lim, Yu-Mi / Yue, Jessica T Y / Lam, Tony K T

iScience

2021 Volume 24, Issue 4, Page(s) 102366

Abstract: Hypothalamic regulation of lipid and glucose homeostasis is emerging, but whether the dorsal vagal complex (DVC) senses nutrients and regulates hepatic nutrient metabolism remains unclear. Here, we found in rats DVC oleic acid infusion suppressed hepatic ...

Abstract	Hypothalamic regulation of lipid and glucose homeostasis is emerging, but whether the dorsal vagal complex (DVC) senses nutrients and regulates hepatic nutrient metabolism remains unclear. Here, we found in rats DVC oleic acid infusion suppressed hepatic secretion of triglyceride-rich very-low-density lipoprotein (VLDL-TG), which was disrupted by inhibiting DVC long-chain fatty acyl-CoA synthetase that in parallel disturbed lipid homeostasis during intravenous lipid infusion. DVC glucose infusion elevated local glucose levels similarly as intravenous glucose infusion and suppressed hepatic glucose production. This was independent of lactate metabolism as inhibiting lactate dehydrogenase failed to disrupt glucose sensing and neither could DVC lactate infusion recapitulate glucose effect. DVC oleic acid and glucose infusion failed to lower VLDL-TG secretion and glucose production in high-fat fed rats, while inhibiting DVC farnesoid X receptor enhanced oleic acid but not glucose sensing. Thus, an impairment of DVC nutrient sensing may lead to the disruption of lipid and glucose homeostasis in metabolic syndrome.
Language	English
Publishing date	2021-03-26
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2021.102366
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Article ; Online: Role of autophagy in diabetes and endoplasmic reticulum stress of pancreatic β-cells.

Quan, Wenying / Lim, Yu Mi / Lee, Myung Shik

Experimental & molecular medicine

2012 Volume 44, Issue 2, Page(s) 81–88

Abstract: Type 2 diabetes mellitus is characterized by insulin resistance and failure of pancreatic β-cells producing insulin. Autophagy plays a crucial role in cellular homeostasis through degradation and recycling of organelles such as mitochondria or ... ...

Abstract	Type 2 diabetes mellitus is characterized by insulin resistance and failure of pancreatic β-cells producing insulin. Autophagy plays a crucial role in cellular homeostasis through degradation and recycling of organelles such as mitochondria or endoplasmic reticulum (ER). Here we discussed the role of β-cell autophagy in development of diabetes, based on our own studies using mice with β-cell-specific deletion of Atg7 (autophagy-related 7 ), an important autophagy gene, and studies by others. β-cell-specific Atg7-null mice showed reduction in β-cell mass and pancreatic insulin content. Insulin secretory function ex vivo was also impaired, which might be related to organelle dysfunction associated with autophagy deficiency. As a result, β-cell-specific Atg7-null mice showed hypoinsulinemia and hyperglycemia. However, diabetes never developed in those mice. Obesity and/or lipid are physiological ER stresses that can precipitate β-cell dysfunction. Our recent studies showed that β-cellspecific Atg7-null mice, when bred with ob/ob mice, indeed become diabetic. Thus, autophagy deficiency in β-cells could be a precipitating factor in the progression from obesity to diabetes due to inappropriate response to obesity-induced ER stress.
MeSH term(s)	Animals ; Autophagy/genetics ; Autophagy/physiology ; Diabetes Mellitus/genetics ; Diabetes Mellitus/metabolism ; Endoplasmic Reticulum Stress/genetics ; Endoplasmic Reticulum Stress/physiology ; Humans ; Insulin-Secreting Cells/metabolism
Language	English
Publishing date	2012-01-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1328915-9
ISSN	2092-6413 ; 1226-3613 ; 0378-8512
ISSN (online)	2092-6413
ISSN	1226-3613 ; 0378-8512
DOI	10.3858/emm.2012.44.2.030
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Zs.A 4775: Show issues

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Article ; Online: TFEB-GDF15 axis protects against obesity and insulin resistance as a lysosomal stress response.

Kim, Jinyoung / Kim, Seong Hun / Kang, Hyereen / Lee, Soyeon / Park, Shi-Young / Cho, Yoonil / Lim, Yu-Mi / Ahn, Ji Woong / Kim, Young-Hwan / Chung, Seungsoo / Choi, Cheol Soo / Jang, Yeon Jin / Park, Hye Soon / Heo, Yoonseok / Kim, Kook Hwan / Lee, Myung-Shik

Nature metabolism

2021 Volume 3, Issue 3, Page(s) 410–427

Abstract: TFEB, a key regulator of lysosomal biogenesis and autophagy, is induced not only by nutritional deficiency but also by organelle stress. Here, we find that Tfeb and its downstream genes are upregulated together with lipofuscin accumulation in adipose ... ...

Abstract	TFEB, a key regulator of lysosomal biogenesis and autophagy, is induced not only by nutritional deficiency but also by organelle stress. Here, we find that Tfeb and its downstream genes are upregulated together with lipofuscin accumulation in adipose tissue macrophages (ATMs) of obese mice or humans, suggestive of obesity-associated lysosomal dysfunction/stress in ATMs. Macrophage-specific TFEB-overexpressing mice display complete abrogation of diet-induced obesity, adipose tissue inflammation and insulin resistance, which is independent of autophagy, but dependent on TFEB-induced GDF15 expression. Palmitic acid induces Gdf15 expression through lysosomal Ca
MeSH term(s)	Adipose Tissue/metabolism ; Animals ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors/genetics ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors/metabolism ; Growth Differentiation Factor 15/metabolism ; Humans ; Insulin Resistance ; Lysosomes/metabolism ; Macrophages/metabolism ; Mice ; Mice, Transgenic ; Obesity/metabolism ; Obesity/prevention & control ; Stress, Physiological
Chemical Substances	Basic Helix-Loop-Helix Leucine Zipper Transcription Factors ; GDF15 protein, human ; Growth Differentiation Factor 15 ; TFEB protein, human
Language	English
Publishing date	2021-03-22
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2522-5812
ISSN (online)	2522-5812
DOI	10.1038/s42255-021-00368-w
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