Evidence map›Paper›PMID 27967236›Full record

ArticleEndocrinology2017

PKA-RIIB Deficiency Induces Brown Fatlike Adipocytes in Inguinal WAT and Promotes Energy Expenditure in Male FVB/NJ Mice.

Jing Su, Wei Wu, Shan Huang, Ruidan Xue, Yi Wang, Yun Wan, Lv Zhang, Lang Qin, Qiongyue Zhang, Xiaoming Zhu and 4 more

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Endocrinology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.6field-weighted citation impact, top 27% 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

9 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. RIIβ-PKA in GABAergic Neurons of Dorsal Median Hypothalamus Governs White Adipose Browning.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Article
  5. Article
  6. Article
  7. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 2 institutions in 1 country.

Jing SuDepartment of Endocrinology and Metabolism, Huashan Hospital, Fudan University, Shanghai, China.
Wei WuDepartment of Endocrinology and Metabolism, Huashan Hospital, Fudan University, Shanghai, China.
Shan HuangDepartment of Endocrinology and Metabolism, Huashan Hospital, Fudan University, Shanghai, China.
Ruidan XueDepartment of Endocrinology and Metabolism, Huashan Hospital, Fudan University, Shanghai, China.
Yi WangDepartment of Endocrinology and Metabolism, Huashan Hospital, Fudan University, Shanghai, China.
Yun WanDepartment of Endocrinology and Metabolism, Huashan Hospital, Fudan University, Shanghai, China.
Lv ZhangDepartment of Endocrinology and Metabolism, Huashan Hospital, Fudan University, Shanghai, China.
Lang QinDepartment of Endocrinology and Metabolism, Huashan Hospital, Fudan University, Shanghai, China.
Qiongyue ZhangDepartment of Endocrinology and Metabolism, Huashan Hospital, Fudan University, Shanghai, China.
Xiaoming ZhuDepartment of Endocrinology and Metabolism, Huashan Hospital, Fudan University, Shanghai, China.
Zhaoyun ZhangDepartment of Endocrinology and Metabolism, Huashan Hospital, Fudan University, Shanghai, China.
Hongying YeDepartment of Endocrinology and Metabolism, Huashan Hospital, Fudan University, Shanghai, China.
Xiaohui WuInstitute of Developmental Biology and Molecular Medicine, School of Life Sciences, Fudan University, Shanghai, China.
Yiming LiDepartment of Endocrinology and Metabolism, Huashan Hospital, Fudan University, Shanghai, China.
Huashan Hospital · CNFudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Obesity has become the most common metabolic disorder worldwide. Promoting brown adipose tissue (BAT) and beige adipose tissue formation, and therefore, a functional increase in energy expenditure, may counteract obesity. Mice lacking type IIβ regulatory subunit of adenosine 3',5' cyclic monophosphate (cAMP)-dependent protein kinase A (PKA-RIIB) display reduced adiposity and resistance to diet-induced obesity. PKA-RIIB, encoded by the Prkar2b gene, is most abundant in BAT and white adipose tissue (WAT) and in the brain. In this study, we show that mice lacking PKA-RIIB have increased energy expenditure, limited weight gain, and improved glucose metabolism. PKA-RIIB deficiency induces brownlike adipocyte in inguinal WAT (iWAT). PKA-RIIB deficiency also increases the expression of uncoupling protein 1 and other thermogenic genes in iWAT and primary preadipocytes from iWAT through a mechanism involving increased PKA activity, which is represented by increased phosphorylation of PKA substrate, cAMP response element binding protein, and P38 mitogen-activated protein kinase. Our study provides evidence for the role of PKA-RIIB deficiency in regulating thermogenesis in WAT, which may potentially have therapeutic implications for the treatment of obesity and related metabolic disorders.

Indexed as

Adipocytes, BrownEnergy MetabolismThermogenesisAdipose Tissue, WhiteAnimalsCarbohydrate MetabolismCyclic AMP-Dependent Protein Kinase RIIbeta SubunitCyclic AMP Response Element-Binding ProteinEpididymisGlucoseLipid MetabolismMaleMiceObesityp38 Mitogen-Activated Protein KinasesUncoupling Protein 1Creb1 protein, mouseCyclic AMP-Dependent Protein Kinase RIIbeta SubunitCyclic AMP Response Element-Binding ProteinGlucosep38 Mitogen-Activated Protein KinasesUcp1 protein, mouseUncoupling Protein 1

Identifiers

PMID27967236
OpenAlexW2563274013

What OpenQuestion holds

Textmetadata
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.