ArticleEndocrinology2011
Sexually dimorphic diet-induced insulin resistance in obese tissue inhibitor of metalloproteinase-2 (TIMP-2)-deficient mice.
Article in Endocrinology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 44 citations in OpenAlex.
- Proteomic Analysis of Tear Films in Healthy Female and Male Dogs Using MALDI-TOF (Matrix Assisted Laser Desortion/Ionization Time-of-Flight) Mass Spectrometry.Animals : an open access journal from MDPI · 2025Article
- Lack of adipocyte FAM20C improves whole body glucose homeostasis.Physiological reports · 2024Article
- Macronutrient-differential dietary pattern impacts on body weight, hepatic inflammation, and metabolism.Frontiers in nutrition · 2024Article
- Roles of Matrix Metalloproteinases and Their Natural Inhibitors in Metabolism: Insights into Health and Disease.International journal of molecular sciences · 2023Review
- Berberine remodels adipose tissue to attenuate metabolic disorders by activating sirtuin 3.Acta pharmacologica Sinica · 2022Article
- Omics Approaches in Adipose Tissue and Skeletal Muscle Addressing the Role of Extracellular Matrix in Obesity and Metabolic Dysfunction.International journal of molecular sciences · 2021Review
- Umbilical Cord-Mesenchymal Stem Cell-Conditioned Medium Improves Insulin Resistance in C2C12 Cell.Diabetes & metabolism journal · 2021Article
- Mechanistic Targets and Nutritionally Relevant Intervention Strategies to Break Obesity-Breast Cancer Links.Frontiers in endocrinology · 2021Review
- Adipose Tissue and Endocrine-Disrupting Chemicals: Does Sex Matter?International journal of environmental research and public health · 2020Review
- Extracellular Matrix Remodeling of Adipose Tissue in Obesity and Metabolic Diseases.International journal of molecular sciences · 2019Review
- Metabolic Phenotype of Wild-Type andEnvironmental health perspectives · 2018Article
- Absence of Tissue Inhibitor of Metalloproteinase-4 (TIMP4) ameliorates high fat diet-induced obesity in mice due to defective lipid absorption.Scientific reports · 2017Article
- FAK signalling controls insulin sensitivity through regulation of adipocyte survival.Nature communications · 2017Article
- High-fat diet-induced obesity regulates MMP3 to modulate depot- and sex-dependent adipose expansion in C57BL/6J mice.American journal of physiology. Endocrinology and metabolism · 2017Article
- Adipose extracellular matrix remodelling in obesity and insulin resistance.Biochemical pharmacology · 2016Review
- Novel Role for Matrix Metalloproteinase 9 in Modulation of Cholesterol Metabolism.Journal of the American Heart Association · 2016Article
- Article
- Emergence of a metalloproteinase / phospholipase A2 axis of systemic inflammation.Metalloproteinases in medicine · 2015Article
- The extracellular matrix and insulin resistance.Trends in endocrinology and metabolism: TEM · 2015Review
- The cell biology of fat expansion.The Journal of cell biology · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
Circulating levels of matrix metalloproteinases (MMPs) and their endogenous inhibitors, tissue inhibitor of metalloproteinases (TIMPs), are altered in human obesity and may contribute to its pathology. TIMP-2 exerts MMP-dependent (MMP inhibition and pro-MMP-2 activation) and MMP-independent functions. To assess the role of TIMP-2 in a murine model of nutritionally induced obesity, weight gain in wild-type and TIMP-2 deficient [knockout (KO)] mice fed a chow or high-fat diet (HFD) was determined. The effects of diet on glucose tolerance and insulin sensitivity, as well as pancreatic β-cell and adipocyte physiology, were assessed. Chow-fed TIMP-2 KO mice of both sexes became obese but maintained relatively normal glucose tolerance and insulin sensitivity. Obesity was exacerbated on the HFD. However, HFD-fed male, but not female, TIMP-2 KO mice developed insulin resistance with reduced glucose transporter 2 and pancreatic and duodenal homeobox 1 levels, despite increased β-cell mass and hyperplasia. Thus, although β-cell mass was increased, HFD-fed male TIMP-2 KO mice develop diabetes likely due to β-cell exhaustion and failure. TIMP-2 mRNA, whose expression was greatest in sc adipose tissue, was down-regulated in HFD-fed wild-type males, but not females. Furthermore, HFD increased membrane type 1-MMP (MMP-14) expression and activity in male, but not female, sc adipose tissue. Strikingly, MMP-14 expression increased to a greater extent in TIMP-2 KO males and was associated with decreased adipocyte collagen. Taken together, these findings demonstrate a role for TIMP-2 in maintaining extracellular matrix integrity necessary for normal β-cell and adipocyte physiology and that loss of extracellular matrix integrity may underlie diabetic and obesogenic phenotypes.
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.