Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (794 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A pathological state in which blood glucose level is less than approximately 140 mg/100 ml of plasma at fasting, and above approximately 200 mg/100 ml plasma at 30-, 60-, or 90-minute during a glucose tolerance test. This condition is seen frequently in diabetes mellitus, but also occurs with other diseases and malnutrition.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Glucose Intolerances; Intolerance, Glucose; Intolerances, Glucose; Impaired Glucose Tolerance; Glucose Tolerance, Impaired; Glucose Tolerances, Impaired; Impaired Glucose Tolerances; Tolerance, Impaired Glucose.
Where it fits in the MeSH classification
- Broader topics
- Hyperglycemia
- See also
- Diabetes Mellitus; Glucose Tolerance Test
Related concepts
- Blood Glucose
- Plasma
- Glucose Tolerance Test
- Diabetes Mellitus
- Malnutrition
Research landscape
PubMed indexes 10,543 records tagged with the MeSH heading “Glucose Intolerance” (counts retrieved 2026-10-31). 1,830 of them (17.4%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 4,561 records.
Reviews account for 1,121 records (10.6%) and meta-analyses for 95. Randomized controlled trials number 683 (6.5%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 868 |
| 2000-2009 | 3,284 |
| 2010-2019 | 4,561 |
| 2020 onward | 1,830 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 1,121 | 10.6% |
| Meta-analyses | 95 | 0.9% |
| Randomized controlled trials | 683 | 6.5% |
Method: PubMed query "Glucose Intolerance"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in metabolism and endocrine disease
Studies of diabetes, obesity and hormone disorders often follow blood tests such as glucose, HbA1c or hormone levels, which are stand-ins for outcomes that matter more, such as complications. Lifestyle and diet research is largely observational, and weight and diabetes trials can differ in how long people were followed. Nothing on this page is advice about medicines, insulin or diet; talk to a qualified clinician about your own situation. Check whether the outcome was a lab value or a clinical event, and the type and duration of the condition studied.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Are HOMA-IR and HOMA-B good predictors for diabetes and pre-diabetes subtypes? | 2023 | Research article Design not recorded in structured metadata | 72 | cc by PMID 36788521 · DOI · PMC9926772 |
| Lifestyle-, environmental-, and additional health factors associated with an increased sperm DNA fragmentation: a systematic review and meta-analysis | 2023 | Meta-analysis Design not recorded in structured metadata | 68 | cc by PMID 36653793 · DOI · PMC9847125 |
| Short-term tamoxifen administration improves hepatic steatosis and glucose intolerance through JNK/MAPK in mice | 2023 | Research article Design not recorded in structured metadata | 47 | cc by PMID 36864030 · DOI · PMC9981902 |
| Impaired glucose tolerance and mild diabetes induce β-cell dysfunction in mice | 2026 | Research article Design not recorded in structured metadata | 1 | cc by PMID 42062260 · DOI · PMC13338056 |
Are HOMA-IR and HOMA-B good predictors for diabetes and pre-diabetes subtypes? [1]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundTo investigate the association between the Homeostasis Model Assessment of Insulin Resistance (HOMA-IR) and Homeostasis Model Assessment of Beta-cell function (HOMA-B) with the incidence of diabetes and pre-diabetes subtypes.
- Closing excerpt
- However, none of these alone is a good criterion for predicting diabetes and pre-diabetes.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (198 words)
BackgroundTo investigate the association between the Homeostasis Model Assessment of Insulin Resistance (HOMA-IR) and Homeostasis Model Assessment of Beta-cell function (HOMA-B) with the incidence of diabetes and pre-diabetes subtypes.MethodsA total of 3101 normoglycemic people aged 20-70 years were included in the 6-year follow-up study. Multinomial logistic regression was used to calculate the incidence possibility of isolated Impaired Fasting Glucose (iIFG), isolated Impaired Glucose Tolerance (iIGT), Combined impaired fasting glucose & impaired glucose tolerance (CGI), and Diabetes Mellitus (DM) per standard deviation (SD) increment in HOMA-IR and HOMA-B in the crude and multivariable model.ResultsIn the multivariate model, an increase in one SD change in HOMA-IR was associated with a 43, 42, 75, and 92% increased risk of iIFG, iIGT, CGI, and DM, respectively. There was a positive correlation between the increase in HOMA-B and the incidence of iIGT; however, after adjusting the results for metabolic syndrome components, it was inversely correlated with the incidence of iIFG [Odds Ratio = 0.86(0.75-0.99)].ConclusionsHOMA-IR is positively correlated with diabetes and pre-diabetes subtypes' incidence, and HOMA-B is inversely correlated with the incidence of iIFG but positively correlated with iIGT incidence. However, none of these alone is a good criterion for predicting diabetes and pre-diabetes.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 36788521 · DOI · PMC9926772
Lifestyle-, environmental-, and additional health factors associated with an increased sperm DNA fragmentation: a systematic review and meta-analysis [2]
Abstract reading summary — source excerpts
- Opening excerpt
- IntroductionInfertility affects one in every six couples in developed countries, and approximately 50% is of male origin.
- Closing excerpt
- Trial registrationCRD42021282533.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (239 words)
IntroductionInfertility affects one in every six couples in developed countries, and approximately 50% is of male origin. In 2021, sperm DNA fragmentation (SDF) testing became an evidence-based test for fertility evaluations depicting fertility more clearly than standard semen parameters. Therefore, we aimed to summarize the potential prognostic factors of a higher SDF.MethodsWe conducted a systematic search in three medical databases and included studies investigating any risk factors for SDF values. We calculated mean differences (MD) in SDF with 95% confidence interval (CI) for exposed and non-exposed individuals.ResultsWe included 190 studies in our analysis. In the group of associated health conditions, varicocele (MD = 13.62%, CI: 9.39-17.84) and impaired glucose tolerance (MD = 13.75%, CI: 6.99-20.51) had the most significant increase in SDF. Among malignancies, testicular tumors had the highest impact, with a maximum of MD = 11.3% (CI: 7.84-14.76). Among infections, the overall effects of both Chlamydia and HPV were negligible. Of lifestyle factors, smoking had the most disruptive effect on SDF - an increase of 9.19% (CI: 4.33-14.06). Different periods of sexual abstinence did not show significant variations in SDF values. Age seemed to have a more drastic effect on SDF from age 50 onwards, with a mean difference of 12.58% (CI: 7.31-17.86). Pollution also had a detrimental effect - 9.68% (CI: 6.85-12.52).ConclusionOf the above risk factors, varicocele, impaired glucose tolerance, testicular tumors, smoking, pollution, and paternal age of over 50 were associated with the highest SDF.Trial registrationCRD42021282533.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 36653793 · DOI · PMC9847125
Short-term tamoxifen administration improves hepatic steatosis and glucose intolerance through JNK/MAPK in mice [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Nonalcoholic fatty liver disease (NAFLD) which is a leading cause of chronic liver diseases lacks effective treatment.
- Closing excerpt
- Pharmacological JNK activator (anisomycin) partially deprived the therapeutic role of tamoxifen in treating hepatic steatosis, proving tamoxifen improved NAFLD in a JNK/MAPK signaling-dependent manner.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (198 words)
Nonalcoholic fatty liver disease (NAFLD) which is a leading cause of chronic liver diseases lacks effective treatment. Tamoxifen has been proven to be the first-line chemotherapy for several solid tumors in clinics, however, its therapeutic role in NAFLD has never been elucidated before. In vitro experiments, tamoxifen protected hepatocytes against sodium palmitate-induced lipotoxicity. In male and female mice fed with normal diets, continuous tamoxifen administration inhibited lipid accumulation in liver, and improved glucose and insulin intolerance. Short-term tamoxifen administration largely improved hepatic steatosis and insulin resistance, however, the phenotypes manifesting inflammation and fibrosis remained unchanged in abovementioned models. In addition, mRNA expressions of genes related to lipogenesis, inflammation, and fibrosis were downregulated by tamoxifen treatment. Moreover, the therapeutic effect of tamoxifen on NAFLD was not gender or ER dependent, as male and female mice with metabolic disorders shared no difference in response to tamoxifen and ER antagonist (fulvestrant) did not abolish its therapeutic effect as well. Mechanistically, RNA sequence of hepatocytes isolated from fatty liver revealed that JNK/MAPK signaling pathway was inactivated by tamoxifen. Pharmacological JNK activator (anisomycin) partially deprived the therapeutic role of tamoxifen in treating hepatic steatosis, proving tamoxifen improved NAFLD in a JNK/MAPK signaling-dependent manner.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 36864030 · DOI · PMC9981902
Impaired glucose tolerance and mild diabetes induce β-cell dysfunction in mice [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Severe chronic hyperglycaemia ( > 15 mM) causes impaired glycolytic and mitochondrial metabolism in pancreatic β-cells, leading to dramatically reduced insulin secretion and content.
- Closing excerpt
- These findings demonstrate that altered β-cell metabolism is an early event in type 2 diabetes development and highlight a need for therapeutic intervention during prediabetes.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (159 words)
Severe chronic hyperglycaemia ( > 15 mM) causes impaired glycolytic and mitochondrial metabolism in pancreatic β-cells, leading to dramatically reduced insulin secretion and content. However, patients with type 2 diabetes often experience many years of reduced β-cell function and impaired glucose tolerance preceding diabetes diagnosis. It is postulated that β-cell function may be compromised by relatively small changes in glycaemia, initiating a gradual decline that underlies diabetes progression. We therefore investigated the extent to which impaired glucose tolerance and chronic mild hyperglycaemia are detrimental to β-cells. We show that chronic elevation of blood glucose of just 2-3 mM is sufficient to impair β-cell function, causing marked changes in metabolic gene expression and reducing insulin content, metabolic enzyme activity, mitochondrial oxidative phosphorylation and insulin secretion. Smaller but significant changes are produced by impaired glucose tolerance. These findings demonstrate that altered β-cell metabolism is an early event in type 2 diabetes development and highlight a need for therapeutic intervention during prediabetes.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42062260 · DOI · PMC13338056
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Oxidative stress, dysfunctional glucose metabolism and Alzheimer disease [5]
- Research article Current approaches for assessing insulin sensitivity and resistance in vivo: advantages, limitations, and appropriate usage [6]
- Research article Impaired fasting glucose and impaired glucose tolerance: implications for care [7]
- Research article Impaired glucose tolerance, type 2 diabetes and metabolic syndrome in polycystic ovary syndrome: a systematic review and meta-analysis [8]
- Research article Pharmacological and lifestyle interventions to prevent or delay type 2 diabetes in people with impaired glucose tolerance: systematic review and meta-analysis [9]
- Research article Molecular mechanisms of lipotoxicity and glucotoxicity in nonalcoholic fatty liver disease [10]
References
- Khalili D, Khayamzadeh M, Kohansal K, Ahanchi NS, Hasheminia M, Hadaegh F, et al.. Are HOMA-IR and HOMA-B good predictors for diabetes and pre-diabetes subtypes?. . 2023. PMID 36788521 · DOI · PMC9926772
- Szabó A, Váncsa S, Hegyi P, Váradi A, Forintos A, Filipov T, et al.. Lifestyle-, environmental-, and additional health factors associated with an increased sperm DNA fragmentation: a systematic review and meta-analysis. . 2023. PMID 36653793 · DOI · PMC9847125
- Fang Z, Xu H, Duan J, Ruan B, Liu J, Song P, et al.. Short-term tamoxifen administration improves hepatic steatosis and glucose intolerance through JNK/MAPK in mice. . 2023. PMID 36864030 · DOI · PMC9981902
- Haythorne E, Lloyd M, Smith CA, van de Bunt M, Rohm M, Elphick A, et al.. Impaired glucose tolerance and mild diabetes induce β-cell dysfunction in mice. . 2026. PMID 42062260 · DOI · PMC13338056
- Butterfield DA, Halliwell B. Oxidative stress, dysfunctional glucose metabolism and Alzheimer disease. Nat Rev Neurosci. 2019. PMID 30737462 · DOI · PMC9382875
- Muniyappa R, Lee S, Chen H, Quon MJ, Quon MJ. Current approaches for assessing insulin sensitivity and resistance in vivo: advantages, limitations, and appropriate usage. Am J Physiol Endocrinol Metab. 2008. PMID 17957034 · DOI
- Nathan DM, Davidson MB, DeFronzo RA, Heine RJ, Henry RR, Pratley R, et al.. Impaired fasting glucose and impaired glucose tolerance: implications for care. Diabetes Care. 2007. PMID 17327355 · DOI
- Moran LJ, Misso ML, Wild RA, Norman RJ. Impaired glucose tolerance, type 2 diabetes and metabolic syndrome in polycystic ovary syndrome: a systematic review and meta-analysis. Hum Reprod Update. 2010. PMID 20159883 · DOI
- Gillies CL, Abrams KR, Lambert PC, Cooper NJ, Sutton AJ, Hsu RT, et al.. Pharmacological and lifestyle interventions to prevent or delay type 2 diabetes in people with impaired glucose tolerance: systematic review and meta-analysis. BMJ. 2007. PMID 17237299 · DOI · PMC1796695
- Mota M, Banini BA, Cazanave SC, Sanyal AJ. Molecular mechanisms of lipotoxicity and glucotoxicity in nonalcoholic fatty liver disease. Metabolism. 2016. PMID 26997538 · DOI · PMC4931958
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-11-04; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-11-04.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.