The DOI matches its Crossref record; 99 of the 99 references it cites were found in a registry or an index.
Contributions of β-Cell Dysfunction and Insulin Resistance to the Pathogenesis of Impaired Glucose Tolerance and Impaired Fasting Glucose
Open accessAbstract
Impaired glucose tolerance (IGT) and impaired fasting glucose (IFG) are intermediate states in glucose metabolism that exist between normal glucose tolerance and overt diabetes. Epidemiological studies demonstrate that the two categories describe distinct populations with only partial overlap, suggesting that different metabolic abnormalities characterize IGT and IFG. Insulin resistance and impaired β-cell function, the primary defects observed in type 2 diabetes, both can be detected in subjects with IGT and IFG. However, clinical studies suggest that the site of insulin resistance varies between the two disorders. While subjects with IGT have marked muscle insulin resistance with only mild hepatic insulin resistance, subjects with IFG have severe hepatic insulin resistance with normal or near-normal muscle insulin sensitivity. Both IFG and IGT are characterized by a reduction in early-phase insulin secretion, while subjects with IGT also have impaired late-phase insulin secretion. The distinct metabolic features present in subjects with IFG and IGT may require different therapeutic interventions to prevent their progression to type 2 diabetes.
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“However, progressive β-cell failure is required and ultimately responsible for type 2 diabetes to become fully manifest ( 1 , 34 , 35 , 37 , 38 ).”
From Skeletal Muscle Insulin Resistance Is the Primary Defect in Type 2 Diabetes (2009) · cites this paper as [37]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Because the great majority of glucose disposal after intravenous glucose administration occurs in muscle, these results provide strong evidence that insulin resistance in muscle is the earliest demonstrable defect in the natural history of type 2 diabetes, but that the development of overt type 2 diabetes occurs only in those individuals whose β-cells are unable to compensate for the defect in”
From Skeletal Muscle Insulin Resistance Is the Primary Defect in Type 2 Diabetes (2009) · cites this paper as [37]
Experimental — accuracy not yet measuredIn the citing paper
“Fasting glucose is maintained between 3.9 and 5.6 mmol/L37 and the post-meal increases rarely exceed 3 mmol/L.38”
From Prediabetes: a high-risk state for diabetes development (2012) · cites this paper as [37]
In the citing paper
“This is in line with the notion that insulin resistance starts years before diabetes development and that decreased beta-cell function is already present in the prediabetic stage.37,42”
From Prediabetes: a high-risk state for diabetes development (2012) · cites this paper as [37]
In the citing paper
“Studies using different measures of β-cell function have reported severely abnormal (up to 80% decreased) insulin secretion in prediabetic people.37,42,48”
From Prediabetes: a high-risk state for diabetes development (2012) · cites this paper as [37]
In the citing paper
“Both IFG and IGT subjects present with insulin resistance, however the site of insulin resistance is different: High hepatic insulin resistance is a typical finding in IFG with almost normal values in skeletal muscle.38,39,45 In IGT, the main site of insulin resistance is the muscle with only modest changes in liver insulin sensitivity.37,38”
From Prediabetes: a high-risk state for diabetes development (2012) · cites this paper as [37]
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Sorted by citations
DeFronzo, R. A. (2009) · Diabetes · doi:10.2337/db09-9028 · Cited by 3,016
Self-citationPrediabetes: a high-risk state for diabetes development
Tabák, A. G., Herder, C., Rathmann, W., Brunner, E. J., & Kivimäki, M. (2012) · The Lancet · doi:10.1016/s0140-6736(12)60283-9 · Cited by 2,958
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Self-citationSkeletal Muscle Insulin Resistance Is the Primary Defect in Type 2 Diabetes
DeFronzo, R. A., & Tripathy, D. (2009) · Diabetes Care · doi:10.2337/dc09-s302 · Cited by 2,102
Self-citationImpaired Fasting Glucose and Impaired Glucose Tolerance
Nathan, D. M., Davidson, M. B., DeFronzo, R. A., Heine, R. J., Henry, R. R., Pratley, R., & Zinman, B. (2007) · Diabetes Care · doi:10.2337/dc07-9920 · Cited by 1,396
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Metadata
- Authors
- Abdul-Ghani, M. A., Tripathy, D., & DeFronzo, R. A.
- Affiliations
- The University of Texas at San Antonio Health Science Center (US)
- Venue
- Diabetes Care
- Publisher
- American Diabetes Association
- Published
- 2006-05-01
- Volume
- 29
- Issue
- 5
- Pages
- 1130-1139
- ISSN
- 0149-5992 (ISSN-L)
- 1935-5548
- OpenAlex
- W4241031718
- Cited by
- 744
- References
- 93
- Citations by year
- 2026: 30 · 2025: 30 · 2024: 61 · 2023: 54 · 2022: 45 · 2021: 33 · 2020: 39 · 2019: 37 · 2018: 32 · 2017: 44 · 2016: 45 · 2015: 37 · 2014: 35 · 2013: 38 · 2012: 29
- FWCI
- 29.32
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Diabetes Care (publishedVersion)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Keywords
- impaired glucose tolerance, impaired fasting glucose, beta-cell dysfunction, insulin resistance, type 2 diabetes, hepatic insulin resistance, skeletal muscle insulin sensitivity, first-phase insulin secretion, prediabetes, diabetes prevention
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