ArticleDiabetes, metabolic syndrome and obesity : targets and therapy2022
Lysophosphatidylcholine (17:0) Improves HFD-Induced Hyperglycemia & Insulin Resistance: A Mechanistic Mice Model Study.
Article in Diabetes, metabolic syndrome and obesity : targets and therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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.
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.
Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- Reglid: novel glycolipids from Korean red ginseng marc.Journal of ginseng research · 2026Article
- Integrating dietary patterns and metabolomics with machine learning for metabolic syndrome risk assessment in a rural population.NPJ science of food · 2026Article
- Metabolomics reveals LysoPC a C17:0 (LPC 17:0) as candidate biomarker for personalized medicine in morbid obesity.Frontiers in medicine · 2026Article
- Dietary Supplement with Milk that Contains Different β-Caseins Influences Gut Microbiota and Serum Metabolites in Mice.Food science of animal resources · 2025Article
- Diabetes and Sarcopenia: Metabolomic Signature of Pathogenic Pathways and Targeted Therapies.International journal of molecular sciences · 2025Review
- Metabolomics in cardiometabolic diseases: Key biomarkers and therapeutic implications for insulin resistance and diabetes.Journal of internal medicine · 2025Review
- Abdominal obesity in youth: the associations of plasma Lysophophatidylcholine concentrations with insulin resistance.Pediatric research · 2025Article
- Transcriptomics and metabolomics analysis of the pathogenesis of a novel hyperlipidemia-susceptible rat strain.Experimental animals · 2025Article
- GPR35-mediated metabolic reprogramming promotes tumorigenesis in digestive cancers.Frontiers in immunology · 2025Review
- Impact of Phenylketonuria on the Serum Metabolome and Plasma Lipidome: A Study in Early-Treated Patients.Metabolites · 2024Article
- Metabolomic Study of Aging inMetabolites · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: Type 2 diabetes mellitus is characterized by the dysregulation of glucose homeostasis and insulin sensitivity, resulting in hyperglycemia. The exploration of a complex regulatory network in host metabolism homeostasis may raise a novel strategy for the prevention of T2D. A variety of metabolites serve as the endogenous ligand of G protein-coupled receptors (GPCR) and play an important role in the pathophysiological process of T2D and insulin resistance, however, the roles of remaining endogenous metabolites in insulin resistance and GPCRs still need to be explored. Patients and Methods: The effect of LPC (17:0) on hyperglycemia were proved in high fat diet (HFD) mice, and qPCR with Western blot technology was used to verify the downstream targets. Results: Herein, we found that LPC (17:0) reduced blood glucose and alleviated insulin resistance and related metabolic disorders in high-fat diet induced (HFD) mice through activating GLP-1 and promoting insulin secretion. Further, the LPC (17:0) was found to stimulate intestinal GPR120, GPR35 and CALCR, with potential effect on GLP-1 stimulation. Conclusion: The above observation revealed LPC (17:0) as an endogenous protective factor with potential role on GPCRs, and it provided theoretical support for the development of LPC (17:0) as a potent drug candidate or health food additive for insulin resistance and hyperglycemia.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.