Evidence map›Paper›PMID 31551816›Full record

ArticleFrontiers in physiology2019

BCAA Catabolic Defect Alters Glucose Metabolism in Lean Mice.

Ji Wang, Yunxia Liu, Kun Lian, Xinyi Shentu, Junwei Fang, Jing Shao, Mengping Chen, Yibin Wang, Meiyi Zhou, Haipeng Sun

Open access · goldAbstract read
In one paragraph

Article in Frontiers in physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.3field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

34 citing papers in PubMed, 57 citations in OpenAlex.

  1. Review
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  10. Mapping Thrombosis Serum Markers byMolecules (Basel, Switzerland) · 2024
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  11. Article
  12. The role of branched-chain amino acids and their downstream metabolites in mediating insulin resistance.Journal of pharmacy & pharmaceutical sciences : a publication of the Canadian Society for Pharmaceutical Sciences, Societe canadienne des sciences pharmaceutiques · 2024
    Review
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  15. [Effect ofSichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2023
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 4 institutions in 2 countries.

Ji WangDepartment of Pathophysiology, Hongqiao International Institute of Medicine, Tongren Hospital, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yunxia LiuDepartment of Pathophysiology, Hongqiao International Institute of Medicine, Tongren Hospital, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Kun LianDepartment of Cardiology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Xinyi ShentuDepartment of Pathophysiology, Hongqiao International Institute of Medicine, Tongren Hospital, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Junwei FangSchool of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Jing ShaoDepartment of Pathophysiology, Hongqiao International Institute of Medicine, Tongren Hospital, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Mengping ChenDepartment of Pathophysiology, Hongqiao International Institute of Medicine, Tongren Hospital, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yibin WangDepartments of Anesthesiology, Medicine and Physiology, David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, CA, United States.
Meiyi ZhouDepartment of Pathophysiology, Hongqiao International Institute of Medicine, Tongren Hospital, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Haipeng SunDepartment of Pathophysiology, Hongqiao International Institute of Medicine, Tongren Hospital, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Shanghai Jiao Tong University · CNTongren Hospital · CNUniversity of California, Los Angeles · USXijing Hospital · CN

Funding

BCAA Catabolic Defect in HF: Novel Mechanism and Therapeutic TargetR01HL140116 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LI, ZHAOPING · 2018 to 2021
$1.6M
NHLBI NIH HHS R01 HL140116
6 · The paper itself

Abstract

Recent studies show branched-chain amino acid (BCAA) catabolic pathway is defective in obese animals and humans, contributing to the pathogenesis of insulin resistance and diabetes. However, in the context of obesity, various processes including the dysfunctional lipid metabolism can affect insulin sensitivity and glycemic regulation. It remains unclear how BCAA catabolic defect may exert direct impacts on glucose metabolism without the disturbance of obesity. The current study characterized the glucose metabolism in lean mice in which the genetic deletion of PP2Cm leads to moderate BCAA catabolic defect. Interestingly, compared to the wildtype control, lean PP2Cm deficient mice showed enhanced insulin sensitivity and glucose tolerance, lower body weight, and the preference for carbohydrate over lipids utilization. Metabolomics profiling of plasma and tissues revealed significantly different metabolic patterns in the PP2Cm deficient mice, featured by the marked alterations in glucose metabolic processes, including gluconeogenesis/glycolysis, glycogen metabolism, and tricarboxylic acid cycle. The metabolic changes of glucose were predominantly observed in liver but not skeletal muscle or white adipose tissue. The elevated branched-chain keto acids (BCKAs) resulted from the BCAA catabolic defect may play a critical role in regulating the expression of key regulators of glucose metabolic processes and the activity of respiratory Complex II/succinate dehydrogenase in TCA cycle. Together, these results show BCAA catabolic defect significantly alters glucose metabolism in lean mice with some impacts different or even opposite from those in obese mice, highlighting the critical role of BCAA catabolism in glycemic regulation and the complex interplay between macronutrients in lean and obese animals.

Indexed as

branched-chain amino acidscatabolic defectglucose metabolismlean miceliver

Identifiers

PMID31551816
PMCPMC6738029
OpenAlexW2969632674

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.