Evidence map›Paper›PMID 33987348›Full record

ArticleAnnals of translational medicine2021

Residual β-cell function after 10 years of autoimmune type 1 diabetes: prevalence, possible determinants, and implications for metabolism.

Jin Cheng, Min Yin, Xiaohan Tang, Xiang Yan, Yuting Xie, Binbin He, Xia Li, Zhiguang Zhou

Open access · diamondAbstract read
In one paragraph

Article in Annals of translational medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

8 citing papers in PubMed, 11 citations in OpenAlex.

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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

8 authors at 2 institutions in 1 country.

Jin ChengNational Clinical Research Center for Metabolic Disease, Key Laboratory of Diabetes Immunology, Ministry of Education, Department of Metabolism and Endocrinology, The Second Xiangya Hospital of Central South University, Changsha, China.
Min YinNational Clinical Research Center for Metabolic Disease, Key Laboratory of Diabetes Immunology, Ministry of Education, Department of Metabolism and Endocrinology, The Second Xiangya Hospital of Central South University, Changsha, China.
Xiaohan TangNational Clinical Research Center for Metabolic Disease, Key Laboratory of Diabetes Immunology, Ministry of Education, Department of Metabolism and Endocrinology, The Second Xiangya Hospital of Central South University, Changsha, China.
Xiang YanNational Clinical Research Center for Metabolic Disease, Key Laboratory of Diabetes Immunology, Ministry of Education, Department of Metabolism and Endocrinology, The Second Xiangya Hospital of Central South University, Changsha, China.
Yuting XieNational Clinical Research Center for Metabolic Disease, Key Laboratory of Diabetes Immunology, Ministry of Education, Department of Metabolism and Endocrinology, The Second Xiangya Hospital of Central South University, Changsha, China.
Binbin HeNational Clinical Research Center for Metabolic Disease, Key Laboratory of Diabetes Immunology, Ministry of Education, Department of Metabolism and Endocrinology, The Second Xiangya Hospital of Central South University, Changsha, China.
Xia LiNational Clinical Research Center for Metabolic Disease, Key Laboratory of Diabetes Immunology, Ministry of Education, Department of Metabolism and Endocrinology, The Second Xiangya Hospital of Central South University, Changsha, China.
Zhiguang ZhouNational Clinical Research Center for Metabolic Disease, Key Laboratory of Diabetes Immunology, Ministry of Education, Department of Metabolism and Endocrinology, The Second Xiangya Hospital of Central South University, Changsha, China.
Central South University · CNSecond Xiangya Hospital of Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundType 1 diabetes (T1D) has long been considered a progressive autoimmune disease resulting in the failure of pancreatic β-cell function and absolute endogenous insulin deficiency. However, several studies have demonstrated patients with T1D have detectable C-peptide levels long after diagnosis, which has remarkable clinical significance. Since this issue has not been systematically explored in non-Caucasian populations, we aimed to identify the prevalence of residual β-cell function and its related clinical features in Chinese long-term T1D patients.

methodsWe enrolled 109 patients with T1D for ≥10 years and administered a mixed-meal tolerance test (MMTT). Fasting and postprandial C-peptide (FCP/PCP) levels were measured to evaluate the insulin secretion function of β-cells. Patients whose FCP and PCP levels were both below the lower detection limit (16.7 pmol/L) were grouped as 'β-cell function depleted', while others were thought to have 'residual β-cell function'. Demographic data, metabolic status, and diabetic complications were compared between patients with or without residual β-cell function.

results38.5% of subjects retained residual β-cell function, and among those, 33.3% responded to MMTT by a two-fold or greater rise of their FCP levels. Clinical features associated with residual β-cell function were older age of diagnosis [27.5 (interquartile range:11.5-37.0)

conclusionsResidual β-cell function can be found in nearly 40% of long-term patients with T1D in China and is associated with older age at diagnosis and better glucose control. The relationship between residual β-cell function and chronic diabetic complications remains to be explored.

Indexed as

C-peptideType 1 diabetes (T1D)β-cell function

Identifiers

PMID33987348
PMCPMC8106063
OpenAlexW3137888669

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

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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.