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Cited by 746Pancreatic function and diabetesDiabetes, Cardiovascular Risks, and LipoproteinsDiabetes Treatment and Management

Contributions of β-Cell Dysfunction and Insulin Resistance to the Pathogenesis of Impaired Glucose Tolerance and Impaired Fasting Glucose

Open access
Abdul-Ghani, Muhammad A., Tripathy, Devjit, DeFronzo, Ralph A.·2006·Diabetes Care
DOI 10.2337/dc05-2179
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Abstract

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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  • Progressive β-cell failure is required and ultimately responsible for type 2 diabetes to become fully manifest.

    “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]

    The ‘Insulin Secretion in IGT and IFG’ section says reduced first-phase insulin secretion predicts progression from normal glucose tolerance to impaired glucose tolerance and then type 2 diabetes. The paper also describes insulin resistance as a contributor; it does not establish that progressive β-cell failure is required or ultimately responsible for overt diabetes. The indexed passages provide no page number for that section. (LLM, conf=0.82)

    Experimental — accuracy not yet measured

  • Insulin resistance in muscle is the earliest demonstrable defect in the natural history of type 2 diabetes, but overt type 2 diabetes occurs only in individuals whose β-cells cannot compensate.

    “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]

    The section on insulin resistance in IGT and IFG says muscle insulin resistance can precede overt diabetes, and the section on insulin secretion describes how increased β-cell output can compensate for reduced insulin sensitivity. But the paper does not establish muscle insulin resistance as the earliest defect for everyone: it describes isolated IFG as primarily involving hepatic resistance, often with normal muscle sensitivity. The categorical claim that overt diabetes occurs only when β-cells fail to compensate is stronger than the passages establish. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • In healthy people, fasting glucose is maintained between 3.9 and 5.6 mmol/L and post-meal increases rarely exceed 3 mmol/L.

    “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]

  • Insulin resistance starts years before diabetes development and decreased beta-cell function is already present in the prediabetic stage.

    “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]

  • Studies using different measures of β-cell function have reported severely abnormal insulin secretion, up to 80% decreased, in prediabetic people.

    “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]

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Research works printed but not linked: 2

  1. [28]28. Qiau Q, Hu G, Tuomilehto J, Balkau B, Bord-Johnsen K, for the DECODE Study Group: Age and sex specific prevalence of diabetes and impaired glucose regula- tion in 13 European cohorts. In Proceed- ings of the 37th Annual Meeting of the European Diabetes Epidemiology Group, 2002. Oxford, U.K., European Diabetes Epidemiology Group, 2002, p. A37
  2. [48]48. Abdul-Ghani MA, Tripathy D, Jenckin- son C, Ritchardson D, DeFronzo RA: In- sulin secretion and insulin action in subjects with impaired fasting glucose and impaired glucose tolerance: results from the Veterans Administration Ge- netic Epidemiology Study (VEGAS). Di- abetes. In press

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Related

Authors
Abdul-Ghani, M. A., Tripathy, D., & DeFronzo, R. A.
Affiliations
The University of Texas at San Antonio Health Science Center (US)
ORCID
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
DOI
10.2337/dc05-2179
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
Locations
Diabetes Care (publishedVersion)
Topics
  • Health Sciences › Medicine › Surgery › 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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