Evidence map›Paper›PMID 42678047›Full record

ArticleAmerican journal of physiology. Endocrinology and metabolism2026

Adipocyte β3-adrenergic receptor signaling attenuates leptin production but is dispensable for fasting induced leptin suppression.

Samuel R Heaselgrave, Steven C Wyler, Shreya Thomas, Arely Tinajero, Marco Galvan, Emma Mihaila, Roger Fan, Teppei Fujikawa, Philipp E Scherer, Joel K Elmquist

Abstract read
In one paragraph

Article in American journal of physiology. Endocrinology and metabolism, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Samuel R HeaselgraveCenter for Hypothalamic Research, Department of Internal Medicine, UT Southwestern Medical Center, Dallas, Texas, United States.ORCID 0009-0001-1749-9229
Steven C WylerCenter for Hypothalamic Research, Department of Internal Medicine, UT Southwestern Medical Center, Dallas, Texas, United States.
Shreya ThomasCenter for Hypothalamic Research, Department of Internal Medicine, UT Southwestern Medical Center, Dallas, Texas, United States.
Arely TinajeroCenter for Hypothalamic Research, Department of Internal Medicine, UT Southwestern Medical Center, Dallas, Texas, United States.
Marco GalvanCenter for Hypothalamic Research, Department of Internal Medicine, UT Southwestern Medical Center, Dallas, Texas, United States.
Emma MihailaCenter for Hypothalamic Research, Department of Internal Medicine, UT Southwestern Medical Center, Dallas, Texas, United States.
Roger FanCenter for Hypothalamic Research, Department of Internal Medicine, UT Southwestern Medical Center, Dallas, Texas, United States.
Teppei FujikawaCenter for Hypothalamic Research, Department of Internal Medicine, UT Southwestern Medical Center, Dallas, Texas, United States.
Philipp E SchererTouchstone Diabetes Center, Department of Internal Medicine, UT Southwestern Medical Center, Dallas, Texas, United States.ORCID 0000-0003-0680-3392
Joel K ElmquistCenter for Hypothalamic Research, Department of Internal Medicine, UT Southwestern Medical Center, Dallas, Texas, United States.ORCID 0000-0001-6929-6370

Funding

Metabolic Benefits of Leptin ReductionR01DK127274 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI JOEL K. ELMQUIST, PHILIPP E SCHERER · 2021 to 2026
$5.1M
SF1 neurons and sympathetic regulation of glucose homeostasisR01DK100659 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI JOEL K. ELMQUIST · 2014 to 2026
$4.8M
Interactions of Leptin and the Melanocortin SystemR01DK118725 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI JOEL K. ELMQUIST · 2018 to 2026
$3.5M
NEUROANATOMIC MECHANIMS OF LEPTIN ACTIONR01DK053301 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI ELMQUIST, JOEL K · 1998 to 2006
$3.0M
Regulation of obesity-related inflammation by alpha-melanocyte stimulating hormoneR01DK142982 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI JOEL K. ELMQUIST, sarah huen · 2026 to 2026
$813k
HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) 2R01DK100659HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) 2R01DK118725HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) 2R01DK127274NIDDK NIH HHS R01 DK053301NIDDK NIH HHS R01 DK100659NIDDK NIH HHS R01 DK118725NIDDK NIH HHS R01 DK127274NIDDK NIH HHS R01 DK142982
6 · The paper itself

Abstract

Leptin, secreted by adipocytes, conveys the status of peripheral energy stores to the brain to regulate appetite and metabolism. Although sympathetic activation via β3-adrenergic receptors (β3-ARs) has been shown to suppress leptin expression, it remains unclear whether this regulation arises directly within adipocytes or through other populations. In addition, it is unclear whether β3-AR signaling contributes to the fasting-induced reduction in leptin. To address this, we generated a novel

Indexed as

AdipocytesFastingLeptinReceptors, Adrenergic, beta-3Adipose Tissue, WhiteAnimalsMaleMiceMice, Inbred C57BLMice, TransgenicSignal TransductionAdrb3 protein, mouseLeptinReceptors, Adrenergic, beta-3adipocyteleptinsympathetic signalingβ3-adrenergic receptor

Identifiers

PMID42678047
PMCPMC13622890

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.