Evidence map›Paper›PMID 31137828›Full record

ArticleNutrients2019

Sulforaphane Prevents Hepatic Insulin Resistance by Blocking Serine Palmitoyltransferase 3-Mediated Ceramide Biosynthesis.

Wendi Teng, Yuan Li, Min Du, Xingen Lei, Siyu Xie, Fazheng Ren

Open access · goldAbstract read
In one paragraph

Article in Nutrients, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 2 pooled it
1.8field-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

28 citing papers in PubMed, 2 syntheses or guidelines pooled it, 51 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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    Review
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  16. Article
  17. Review
  18. Review
  19. Sphingolipids in mitochondria-from function to disease.Frontiers in cell and developmental biology · 2023
    Review
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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

6 authors at 4 institutions in 3 countries.

Wendi TengBeijing Advanced Innovation Center for Food Nutrition and Human Health, College of Food Science & Nutritional Engineering, China Agricultural University, Beijing 100083, China. tengwendidi@163.com.ORCID 0000-0002-4135-8901
Yuan LiKey Laboratory of Functional Dairy, Co-constructed by ministry of Education and Beijing Municipality, College of Food Science & Nutritional Engineering, China Agricultural University, Beijing 100083, China. yuanli@cau.edu.cn.
Min DuDepartment of Animal Sciences, Washington State University, Pullman, WA 99164, USA. min.du@wsu.edu.
Xingen LeiDepartment of Animal Science, Cornell University, Ithaca, NY 14853, USA. xl20@cornell.edu.
Siyu XieBeijing Advanced Innovation Center for Food Nutrition and Human Health, College of Food Science & Nutritional Engineering, China Agricultural University, Beijing 100083, China. xiesiyu2406@163.com.
Fazheng RenBeijing Advanced Innovation Center for Food Nutrition and Human Health, College of Food Science & Nutritional Engineering, China Agricultural University, Beijing 100083, China. renfazheng@cau.edu.cn.
China Agricultural University · CNCornell University · USMinistry of Education · SAWashington State University · US

Funding

Beijing Nova Program No. Z181100006218071National Natural Science Foundation of China NSFC 31471577, 31772014
6 · The paper itself

Abstract

Sulforaphane (SFA), a naturally active isothiocyanate compound from cruciferous vegetables used in clinical trials for cancer treatment, was found to possess potency to alleviate insulin resistance. But its underlying molecular mechanisms are still incompletely understood. In this study, we assessed whether SFA could improve insulin sensitivity and glucose homeostasis both in vitro and in vivo by regulating ceramide production. The effects of SFA on glucose metabolism and expression levels of key proteins in the hepatic insulin signaling pathway were evaluated in insulin-resistant human hepatic carcinoma HepG2 cells. The results showed that SFA dose-dependently increased glucose uptake and intracellular glycogen content by regulating the insulin receptor substrate 1 (IRS-1)/protein kinase B (Akt) signaling pathway in insulin-resistant HepG2 cells. SFA also reduced ceramide contents and downregulated transcription of ceramide-related genes. In addition, knockdown of serine palmitoyltransferase 3 (SPTLC3) in HepG2 cells prevented ceramide accumulation and alleviated insulin resistance. Moreover, SFA treatment improved glucose tolerance and insulin sensitivity, inhibited SPTLC3 expression and hepatic ceramide production and reduced hepatic triglyceride content in vivo. We conclude that SFA recovers glucose homeostasis and improves insulin sensitivity by blocking ceramide biosynthesis through modulating SPTLC3, indicating that SFA may be a potential candidate for prevention and amelioration of hepatic insulin resistance via a ceramide-dependent mechanism.

Indexed as

Insulin ResistanceAnimalsCeramidesEnzyme InhibitorsGlucoseGlycogenHepatocytesHep G2 CellsHumansInsulinInsulin Receptor Substrate ProteinsIsothiocyanatesLiverMaleMice, Inbred C57BLPalmitic AcidCeramidesEnzyme InhibitorsGlucoseGlycogenInsulinInsulin Receptor Substrate ProteinsIRS1 protein, humanIsothiocyanatesPalmitic AcidProto-Oncogene Proteins c-aktSerine C-PalmitoyltransferaseSPTLC3 protein, humanSPTLC3 protein, mousesulforaphaneSulfoxidesTriglyceridesceramideglucose uptakeinsulin resistanceliversulforaphane

Identifiers

PMID31137828
PMCPMC6566605
OpenAlexW2947783179

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.