Evidence map›Paper›PMID 37482325›Full record

ReviewPharmacological research2023

Central and peripheral actions of nicotine that influence blood glucose homeostasis and the development of diabetes.

Zuxin Chen, Xin-An Liu, Paul J Kenny

Open access · goldAbstract readReview
In one paragraph

Review in Pharmacological research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
5.1field-weighted citation impact, top 4% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

  1. Pooled it
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  11. Nicotine Reprograms Aging-Related Metabolism and Protects Against Motor Decline in Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
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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

3 authors at 3 institutions in 2 countries.

Zuxin ChenShenzhen Key Laboratory of Drug Addiction, Shenzhen Neher Neural Plasticity Laboratory, The Brain Cognition and Brain Disease Institute, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen, China; University of Chinese Academy of Sciences, Beijing, China; Shenzhen-Hong Kong Institute of Brain Science-Shenzhen Fundamental Research Institutions, Shenzhen, China.
Xin-An LiuGuangdong Provincial Key Laboratory of Brain Connectome and Behavior, CAS Key Laboratory of Brain Connectome and Manipulation, Brain Cognition and Brain Disease Institute (BCBDI), Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen, China; University of Chinese Academy of Sciences, Beijing, China; Shenzhen-Hong Kong Institute of Brain Science-Shenzhen Fundamental Research Institutions, Shenzhen, China. Electronic address: xa.liu@siat.ac.cn.
Paul J KennyNash Family Department of Neuroscience, Icahn School of Medicine at Mount Sinai, New York, USA. Electronic address: Paul.Kenny@mssm.edu.
Chinese Academy of Sciences · CNIcahn School of Medicine at Mount Sinai · USShenzhen Institutes of Advanced Technology · CN

Funding

Role for Tas2Rs in opioid addictionR37DA020686 · NIDA · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI Paul J. Kenny · 2018 to 2026
$3.7M
Habenular immune signaling and addictionR01DA045649 · NIDA · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI KENNY, PAUL J. · 2018 to 2022
$3.1M
Training Program in Substance Use DisordersT32DA053558 · NIDA · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI Paul J. Kenny · 2021 to 2026
$2.6M
Nicotinic receptors and alcohol reinforcementR01AA024292 · NIAAA · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI KENNY, PAUL J. · 2016 to 2020
$1.9M
NIAAA NIH HHS R01 AA024292NIDA NIH HHS R01 DA045649NIDA NIH HHS R37 DA020686NIDA NIH HHS T32 DA053558
6 · The paper itself

Abstract

Cigarette smoking has long been recognized as a risk factor for type 2 diabetes (T2D), although the precise causal mechanisms underlying this relationship remain poorly understood. Recent evidence suggests that nicotine, the primary reinforcing component in tobacco, may play a pivotal role in connecting cigarette smoking and T2D. Extensive research conducted in both humans and animals has demonstrated that nicotine can elevate blood glucose levels, disrupt glucose homeostasis, and induce insulin resistance. The review aims to elucidate the genetic variants of nicotinic acetylcholine receptors associated with diabetes risk and provide a comprehensive overview of the available data on the mechanisms through which nicotine influences blood glucose homeostasis and the development of diabetes. Here we emphasize the central and peripheral actions of nicotine on the release of glucoregulatory hormones, as well as its effects on glucose tolerance and insulin sensitivity. Notably, the central actions of nicotine within the brain, which encompass both insulin-dependent and independent mechanisms, are highlighted as potential targets for intervention strategies in diabetes management.

Indexed as

Diabetes Mellitus, Type 2Insulin ResistanceReceptors, NicotinicAnimalsBlood GlucoseHomeostasisHumansNicotineBlood GlucoseNicotineReceptors, NicotinicCentral-peripheral interactionsGlucoregulatory hormonesNicotine addictionNicotinic acetylcholine receptorsType 2 diabetes

Identifiers

PMID37482325
PMCPMC13183268
OpenAlexW4385077458

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.