ReviewEndocrine2006
Insulin resistance and improvements in signal transduction.
Review in Endocrine, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 104 citations in OpenAlex.
- Glucose Control in Severely Burned Patients Using Metformin: An Interim Safety and Efficacy Analysis of a Phase II Randomized Controlled Trial.Annals of surgery · 2016Trial
- Matrix metalloproteinase-9 is increased in obese subjects and decreases in response to pioglitazone.The Journal of clinical endocrinology and metabolism · 2010Trial
- The Role of the Dysregulated JNK Signaling Pathway in the Pathogenesis of Human Diseases and Its Potential Therapeutic Strategies: A Comprehensive Review.Biomolecules · 2024Review
- Discovery of Orally Bioavailable Purine-Based Inhibitors of the Low-Molecular-Weight Protein Tyrosine Phosphatase.Journal of medicinal chemistry · 2021Article
- Modulation of Insulin Sensitivity by Exercise Training: Implications for Cardiovascular Prevention.Journal of cardiovascular translational research · 2021Review
- Adiponectin Exerts Peripheral Inhibitory Effects on the Mouse Gastric Smooth Muscle through the AMPK Pathway.International journal of molecular sciences · 2020Article
- Dietary Exposure to Transgenic Rice Expressing the Spider Silk Protein Fibroin Reduces Blood Glucose Levels in Diabetic Mice: The Potential Role of Insulin Receptor Substrate-1 Phosphorylation in Adipocytes.Development & reproduction · 2019Article
- Hypoglycemic and hypolipidemic effects of total saponins from Stauntonia chinensis in diabetic db/db mice.Journal of cellular and molecular medicine · 2018Article
- Diabetes reversal by inhibition of the low-molecular-weight tyrosine phosphatase.Nature chemical biology · 2017Article
- The necroptosis-inducing kinase RIPK3 dampens adipose tissue inflammation and glucose intolerance.Nature communications · 2016Article
- Insights into the molecular mechanisms of diabetes-induced endothelial dysfunction: focus on oxidative stress and endothelial progenitor cells.Endocrine · 2015Article
- Metabolic Alterations Associated to Brain Dysfunction in Diabetes.Aging and disease · 2015Review
- Article
- Swim training of monosodium L-glutamate-obese mice improves the impaired insulin receptor tyrosine phosphorylation in pancreatic islets.Endocrine · 2013Article
- The IL-6 Paradox: Context Dependent Interplay of SOCS3 and AMPK.Journal of diabetes & metabolism · 2013Article
- Altered gene expression profiles in the hippocampus and prefrontal cortex of type 2 diabetic rats.BMC genomics · 2012Article
- Article
- Models of carcinogenesis: an overview.Carcinogenesis · 2010Review
- Cellular bioenergetics as a target for obesity therapy.Nature reviews. Drug discovery · 2010Review
- Combining short-term metformin treatment and one bout of exercise does not increase insulin action in insulin-resistant individuals.American journal of physiology. Endocrinology and metabolism · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Type 2 diabetes and obesity are common metabolic disorders characterized by resistance to the actions of insulin to stimulate skeletal muscle glucose disposal. Insulin-resistant muscle has defects at several steps of the insulin-signaling pathway, including decreases in insulin-stimulated insulin receptor and insulin receptor substrate-1 tyrosine phosphorylation, and phosphatidylinositol 3-kinase (PI 3-kinase) activation. One approach to increase muscle glucose disposal is to reverse/improve these insulin-signaling defects. Weight loss and thiazolidinediones (TZDs) improve glucose disposal, in part, by increasing insulin-stimulated insulin receptor and IRS-1 tyrosine phosphorylation and PI 3-kinase activity. In contrast, physical training and metformin improve whole-body glucose disposal but have minimal effects on proximal insulin-signaling steps. A novel approach to reverse insulin resistance involves inhibition of the stress-activated protein kinase Jun N-terminal kinase (JNK) and the protein tyrosine phosphatases (PTPs). A different strategy to increase muscle glucose disposal is by stimulating insulin-independent glucose transport. AMP-activated protein kinase (AMPK) is an enzyme that works as a fuel gauge and becomes activated in situations of energy consumption, such as muscle contraction. Several studies have shown that pharmacologic activation of AMPK increases glucose transport in muscle, independent of the actions of insulin. AMPK activation is also involved in the mechanism of action of metformin and adiponectin. Moreover, in the hypothalamus, AMPK regulates appetite and body weight. The effect of AMPK to stimulate muscle glucose disposal and to control appetite makes it an important pharmacologic target for the treatment of type 2 diabetes and obesity.
Indexed as
Identifiers
What Socratic 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 Socratic graph.