Evidence map›Paper›PMID 25874615›Full record

ArticlePloS one2015

Tang-Nai-Kang alleviates pre-diabetes and metabolic disorders and induces a gene expression switch toward fatty acid oxidation in SHR.Cg-Leprcp/NDmcr rats.

Linyi Li, Hisae Yoshitomi, Ying Wei, Lingling Qin, Jingxin Zhou, Tunhai Xu, Xinli Wu, Tian Zhou, Wen Sun, Xiangyu Guo and 6 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.5field-weighted citation impact, top 30% 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

10 citing papers in PubMed, 23 citations in OpenAlex.

  1. Food & nutrition research · 2024
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  5. Article
  6. Tangnaikang Alleviates Hyperglycemia and Improves Gut Microbiota in Diabetic Mice.Evidence-based complementary and alternative medicine : eCAM · 2021
    Article
  7. Nicotinamide Mononucleotide Combined WithFrontiers in pharmacology · 2021
    Article
  8. Review
  9. Article
  10. Review
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

16 authors at 3 institutions in 2 countries.

Linyi LiHealth-cultivation Laboratory of the Ministry of Education, Beijing University of Chinese Medicine, Beijing, China.
Hisae YoshitomiSchool of Pharmaceutical Sciences, Mukogawa Women's University, Hyogo, Japan.
Ying WeiHealth-cultivation Laboratory of the Ministry of Education, Beijing University of Chinese Medicine, Beijing, China.
Lingling QinHealth-cultivation Laboratory of the Ministry of Education, Beijing University of Chinese Medicine, Beijing, China.
Jingxin ZhouDongzhimen Hospital Eastern Affiliated to Beijing University of Chinese Medicine, Beijing, China.
Tunhai XuHealth-cultivation Laboratory of the Ministry of Education, Beijing University of Chinese Medicine, Beijing, China.
Xinli WuHealth-cultivation Laboratory of the Ministry of Education, Beijing University of Chinese Medicine, Beijing, China.
Tian ZhouDongfang Hospital Affiliated to Beijing University of Chinese Medicine, Beijing, China.
Wen SunHealth-cultivation Laboratory of the Ministry of Education, Beijing University of Chinese Medicine, Beijing, China.
Xiangyu GuoDongfang Hospital Affiliated to Beijing University of Chinese Medicine, Beijing, China.
Lili WuHealth-cultivation Laboratory of the Ministry of Education, Beijing University of Chinese Medicine, Beijing, China.
Haiyan WangHealth-cultivation Laboratory of the Ministry of Education, Beijing University of Chinese Medicine, Beijing, China.
Yan ZhangHealth-cultivation Laboratory of the Ministry of Education, Beijing University of Chinese Medicine, Beijing, China.
Chunna LiHealth-cultivation Laboratory of the Ministry of Education, Beijing University of Chinese Medicine, Beijing, China.
Tonghua LiuHealth-cultivation Laboratory of the Ministry of Education, Beijing University of Chinese Medicine, Beijing, China.
Ming GaoSchool of Pharmaceutical Sciences, Mukogawa Women's University, Hyogo, Japan.
Beijing University of Chinese Medicine · CNMukogawa Women's University · JPDongzhimen Hospital Affiliated to Beijing University of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Increased energy intake and reduced physical activity can lead to obesity, diabetes and metabolic syndrome. Transcriptional modulation of metabolic networks has become a focus of current drug discovery research into the prevention and treatment of metabolic disorders associated with energy surplus and obesity. Tang-Nai-Kang (TNK), a mixture of five herbal plant extracts, has been shown to improve abnormal glucose metabolism in patients with pre-diabetes. Here, we report the metabolic phenotype of SHR.Cg-Leprcp/NDmcr (SHR/cp) rats treated with TNK. Pre-diabetic SHR/cp rats were randomly divided into control, TNK low-dose (1.67 g/kg) and TNK high-dose (3.24 g/kg) groups. After high-dose treatment for 2 weeks, the serum triglycerides and free fatty acids in SHR/cp rats were markedly reduced compared to controls. After 3 weeks of administration, the high dose of TNK significantly reduced the body weight and fat mass of SHR/cp rats without affecting food consumption. Serum fasting glucose and insulin levels in the TNK-treated groups decreased after 6 weeks of treatment. Furthermore, TNK-treated rats exhibited obvious improvements in glucose intolerance and insulin resistance. The improved glucose metabolism may be caused by the substantial reduction in serum lipids and body weight observed in SHR/cp rats starting at 3 weeks of TNK treatment. The mRNA expression of NAD+-dependent deacetylase sirtuin 1 (SIRT1) and genes related to fatty acid oxidation was markedly up-regulated in the muscle, liver and adipose tissue after TNK treatment. Furthermore, TNK promoted the deacetylation of two well-established SIRT1 targets, PPARγ coactivator 1α (PGC1α) and forkhead transcription factor 1 (FOXO1), and induced the phosphorylation of AMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase (ACC) in different tissues. These observations suggested that TNK may be an alternative treatment for pre-diabetes and metabolic syndrome by inducing a gene expression switch toward fat oxidation through the activation of SIRT1 and AMPK signaling.

Indexed as

AMP-Activated Protein KinasesAnimalsBody WeightDiabetes MellitusDrugs, Chinese HerbalEnergy MetabolismFatty Acids, NonesterifiedGene Expression RegulationGlucoseHumansInsulinMetabolic SyndromeRatsSirtuin 1TriglyceridesAMP-Activated Protein KinasesDrugs, Chinese HerbalFatty Acids, NonesterifiedGlucoseInsulinPrkaa1 protein, ratSirt1 protein, ratSirtuin 1Triglycerides

Identifiers

PMID25874615
PMCPMC4395456
OpenAlexW2031220719

What OpenQuestion holds

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LicenceCC BY
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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.