Evidence map›Paper›PMID 27956941›Full record

ArticleDiabetology & metabolic syndrome2016

Accumulation of intestinal tissue 3-deoxyglucosone attenuated GLP-1 secretion and its insulinotropic effect in rats.

Lurong Zhang, Xiudao Song, Liang Zhou, Guoqiang Liang, Heng Xu, Fei Wang, Fei Huang, Guorong Jiang

Open access · goldAbstract read
In one paragraph

Article in Diabetology & metabolic syndrome, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
2.5field-weighted citation impact, top 12% 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

5 citing papers in PubMed, 18 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 1 institution in 1 country.

Lurong Zhang *Suzhou Academy of Wumen Chinese Medicine, Suzhou Hospital of Traditional Chinese Medicine, No. 18, Yangsu Road, Suzhou, 215003 Jiangsu People's Republic of China.
Xiudao Song *Suzhou Academy of Wumen Chinese Medicine, Suzhou Hospital of Traditional Chinese Medicine, No. 18, Yangsu Road, Suzhou, 215003 Jiangsu People's Republic of China.
Liang ZhouSuzhou Academy of Wumen Chinese Medicine, Suzhou Hospital of Traditional Chinese Medicine, No. 18, Yangsu Road, Suzhou, 215003 Jiangsu People's Republic of China.
Guoqiang LiangSuzhou Academy of Wumen Chinese Medicine, Suzhou Hospital of Traditional Chinese Medicine, No. 18, Yangsu Road, Suzhou, 215003 Jiangsu People's Republic of China.
Heng XuSuzhou Academy of Wumen Chinese Medicine, Suzhou Hospital of Traditional Chinese Medicine, No. 18, Yangsu Road, Suzhou, 215003 Jiangsu People's Republic of China.
Fei WangSuzhou Academy of Wumen Chinese Medicine, Suzhou Hospital of Traditional Chinese Medicine, No. 18, Yangsu Road, Suzhou, 215003 Jiangsu People's Republic of China.
Fei HuangSuzhou Academy of Wumen Chinese Medicine, Suzhou Hospital of Traditional Chinese Medicine, No. 18, Yangsu Road, Suzhou, 215003 Jiangsu People's Republic of China.
Guorong JiangSuzhou Academy of Wumen Chinese Medicine, Suzhou Hospital of Traditional Chinese Medicine, No. 18, Yangsu Road, Suzhou, 215003 Jiangsu People's Republic of China.
Suzhou Traditional Chinese Medicine Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundOur recent findings support the idea that 3-deoxyglucosone (3DG), a dietary composition, has been suggested as an independent factor for the development of prediabetes. Secretion of glucagon-like peptide-1 (GLP-1) has been suggested to be impaired in T2DM and in conditions associated with hyperglycemia. Since low oral bioavailability of 3DG has been indicated in a single administration study, in the present study we examined if 3DG is capable of accumulating in intestinal tissue of rats after 2-week administration of 3DG, and the 3DG treatment affects GLP-1 secretion and glucose tolerance.

methodsRats were administered by gastric gavage for 2 weeks. We measured 3DG contents of intestinal tissues (by HPLC), plasma levels of total GLP-1 (by ELISA), insulin and glucagon (both by radioimmunoassay) and blood glucose concentrations. The expressions of the sweet receptor subunits (TAS1R2, TAS1R3) and its downstream molecule TRPM5 in duodenum and colon tissues of rats were quantified by WB. We examined GLP-1 secretion in enteroendocrine STC-1 cells exposured to 3DG.

results3DG treatment for 2 weeks increased 3DG content of intestinal tissues, fasting blood glucose concentration, and reduced plasma concentrations of GLP-1 and insulin at fasting and 15 and 180 min after the glucose load and oral glucose tolerance in conjunction with increased plasma glucagon concentrations. The expressions of TAS1R2, TAS1R3 and TRPM5 were shown to be reduced whereas 3DG treatment did not affect plasma dipeptidyl peptidase-4 activity, indicating an impaired GLP-1 secretion in 3DG-treated rats. This idea was further supported by the fact that exposure to 3DG directly decrease GLP-1 secretion in STC-1.

conclusionIt is the first demonstration that 3DG was capable of accumulating in intestinal tissue and thereby decreased secretion of GLP-1 and insulin in a similar manner. 3DG-treated rats developed impaired glucose regulation (IGR) with obviously pancreatic islet cell dysfunction. It is further concluded that a decrease in the biological function of GLP-1 resulting from the decreased GLP-1 secretion is the most likely mechanism for the impaired insulin secretion, which ultimately promoted the development of IGR. These results will also contribute to a better understanding of the significance for restoring physiological GLP-1 secretion.

Indexed as

3-DeoxyglucosoneGlucagon-like peptide-1Impaired glucose regulationInsulinotropicType 2 diabetes mellitus

Identifiers

PMID27956941
PMCPMC5129672
OpenAlexW2557888760

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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.