Evidence map›Paper›PMID 28257332›Full record

ReviewCurrent opinion in clinical nutrition and metabolic care2017

Parathyroid hormone stimulates adipose tissue browning: a pathway to muscle wasting.

Sandhya S Thomas, William E Mitch

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in clinical nutrition and metabolic care, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 2 pooled it
3.0field-weighted citation impact, top 9% 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

32 citing papers in PubMed, 2 syntheses or guidelines pooled it, 39 citations in OpenAlex.

  1. Serum parathyroid hormone and risk of sarcopenia: a meta-analysis.Journal of orthopaedic surgery and research · 2025
    Pooled it
  2. Pooled it
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  11. Immunoregulation in cancer-associated cachexia.Journal of advanced research · 2024
    Review
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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

2 authors at 1 institution in 1 country.

Sandhya S ThomasaMichael E. Debakey Veterans Affair Medical Center bDivision of Nephrology, Selzman Institute for Kidney Health, Baylor College of Medicine, One Baylor Plaza, Houston, Texas, USA.
William E Mitch
Baylor College of Medicine · US

Funding

PROTEIN NUTRITION IN EXPERIMENTAL UREMIAR01DK037175 · NIDDK · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI Zhaoyong Hu · 1986 to 2026
$4.3M
PROTEIN NUTRITION IN EXPERIMENTAL UREMIAR37DK037175 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI MITCH, WILLIAM EVANS · 2006 to 2015
$3.8M
Chronic_Kidney_Disease_and_Impaired_Actions_of_InsulinIK2BX002492 · VA · MICHAEL E DEBAKEY VA MEDICAL CENTER · PI THOMAS, SANDHYA S · 2015 to 2019
–
BLRD VA IK2 BX002492NIDDK NIH HHS R01 DK037175NIDDK NIH HHS R37 DK037175
6 · The paper itself

Abstract

purpose of reviewStudying organ-to-organ communications (i.e. crosstalk) uncovers mechanisms regulating metabolism in several tissues. What is missing is identification of mediators of different catabolic conditions contributing to losses of adipose and muscle tissues. Identifying mediators involved in organ-to-organ crosstalk could lead to innovative therapeutic strategies because several disorders such as chronic kidney disease (CKD), cancer cachexia, and other catabolic conditions share signals of worsening metabolism and increased risk of mortality. RECENT

findingsA recent breakthrough published in Cell Metabolism leads to the conclusion that parathyroid hormone (PTH) and parathyroid hormone-related peptide (PTHrP) cause 'browning' of white adipose tissue plus energy production via activation of uncoupling protein-1. Browning was associated with muscle wasting in mouse models of cancer and CKD. The pathway to browning includes PTH/PTHrP activation of protein kinase A (PKA) and lost muscle mass via the ubiquitin proteasome proteolytic system (UPS). SUMMARY: The results suggest that crosstalk between muscle and fat contributes in a major way to tissue catabolism. The pathway initiated by PTH or PTHrP is novel and it suggests potential interrelationships that control metabolism in other catabolic conditions. Identifying how the parathyroid hormone-PKA-UPS axis relates to obesity, type 2 diabetes, and other insulin-resistant conditions remains unclear.

Indexed as

Adipose Tissue, BrownAdipose Tissue, WhiteAnimalsCachexiaEnergy MetabolismHumansMiceMuscular AtrophyMuscular DiseasesParathyroid HormoneParathyroid Hormone-Related ProteinProteasome Endopeptidase ComplexRenal Insufficiency, ChronicSignal TransductionUbiquitinsUncoupling Protein 1Parathyroid HormoneParathyroid Hormone-Related ProteinProteasome Endopeptidase ComplexUbiquitinsUncoupling Protein 1

Identifiers

PMID28257332
PMCPMC5822722
OpenAlexW2594084500

What OpenQuestion holds

Textmetadata
LicenceTDM
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.