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Cited by 338Pancreatic function and diabetesDiabetes, Cardiovascular Risks, and LipoproteinsDiabetes Treatment and Management

Beta-cell dysfunction and glucose intolerance: results from the San Antonio metabolism (SAM) study

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Gastaldelli, A., Ferrannini, E., Miyazaki, Y., Matsuda, M., DeFronzo, R. A.·2004·Diabetologia
DOI 10.1007/s00125-003-1263-9
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Abstract

Aims/hypothesis Both insulin resistance and beta-cell dysfunction play a role in the transition from normal glucose tolerance (NGT) to Type 2 diabetes (T2DM) through impaired glucose tolerance (IGT). The aim of the study was to define the level of glycaemia at which beta-cell dysfunction becomes evident in the context of existing insulin resistance.Methods Insulin response (OGTT) and insulin sensitivity (euglycaemic insulin clamp) were evaluated in 388 subjects in the San Antonio Metabolism (SAM) study (138 NGT, 49 IGT and 201 T2DM). In all subjects the insulin secretion/insulin resistance index (DeltaI/DeltaG/IR) was calculated as the ratio of the increment in plasma insulin to the increment in plasma glucose during the OGTT divided by insulin resistance, as measured during the clamp.Results In lean NGTs with a 2-h plasma glucose concentration (2-h PG) between 5.6 and 6.6 and between 6.7 and 7.7 mmol/l, there was a progressive decline in DeltaI/DeltaG/IR compared with NGTs with a 2-h PG less than 5.6 mmol/l. There was a further decline in DeltaI/DeltaG/IR in IGTs with a 2-h PG between 7.8 and 9.3 and between 9.4 and 11.0 mmol/l, and in Type 2 diabetic patients with a 2-h PG greater than 11.1 mmol/l. Lean and obese subjects showed coincident patterns of relation of 2-h PG to DeltaI/DeltaG/IR.Conclusion/interpretation When the plasma insulin response to oral glucose is related to the glycaemic stimulus and severity of insulin resistance, there is a progressive decline in beta-cell function that begins in "normal" glucose tolerant individuals.

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  • Insulin delivered into the portal vein is a major regulator of hepatic glucose production, and people with obesity, prediabetes, and type 2 diabetes have increased gluconeogenesis and impaired insulin suppression of hepatic glucose production.

    “Furthermore, insulin delivered into the portal vein is a major regulator of hepatic glucose production (HGP) and people with obesity, prediabetes, and type 2 diabetes have increased gluconeogenesis and an impairment in the capacity of insulin to suppress HGP 4, 5.”

    From Effect of exercise training on insulin-stimulated glucose disposal: A systematic review and meta-analysis of randomized controlled trials (2023) · cites this paper as [4]

    Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

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  • 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 [38]

    The introductory passage (indexed as Abstract; page unavailable) describes insulin resistance before impaired glucose regulation, and the Discussion says overt type 2 diabetes develops when β-cell secretion cannot offset that resistance. The paper does not establish that resistance specifically in muscle is the earliest demonstrable defect; its Discussion also reports β-cell dysfunction in people whose glucose tolerance remains normal. (LLM, conf=0.84)

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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 [38]

  • 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 [42]

  • 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 [42]

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Research works printed but not linked: 1

  1. [27]27. Ahren B, Taborsky GJ (2003) Beta-cell function and insu- lin secretion. In: Porte D, Sherwin RS, Baron A (eds) Ellenberg Rifkins diabetes mellitus. McGraw Hill, New York, pp 43-65

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Authors
Gastaldelli, A., Ferrannini, E., Miyazaki, Y., Matsuda, M., & DeFronzo, R. A.
Affiliations
  • Istituto di Fisiologia Clinica (IT)
  • University of Pisa (IT)
  • The University of Texas at San Antonio Health Science Center (US)
Corresponding author
DeFronzo, R. A.
ORCID
Venue
Diabetologia
Publisher
Springer Science and Business Media LLC
Published
2004-01-01
Volume
47
Issue
1
Pages
31-39
ISSN
  • 0012-186X (ISSN-L)
  • 1432-0428
DOI
10.1007/s00125-003-1263-9
OpenAlex
W2170932033
Semantic Scholar
4d16abf220df3be3a870cd3062701f66dfcf8289
Cited by
338
References
66
Citations by year
2026: 4 · 2025: 10 · 2024: 11 · 2023: 9 · 2022: 11 · 2021: 17 · 2020: 23 · 2019: 12 · 2018: 15 · 2017: 20 · 2016: 16 · 2015: 17 · 2014: 19 · 2013: 23 · 2012: 15
FWCI
13.58
Type
journal article
Language
en
Open access
Licence
www.springer.com/tdm (tdm)
Locations
  • Diabetologia (publishedVersion)
  • PubMed (publishedVersion)
  • CINECA IRIS Institutial research information system (University of Pisa) (submittedVersion)
Funders
  • Deutsches Krebsforschungszentrum
  • European Foundation for the Study of Diabetes
  • Novo Nordisk
  • National Institutes of Health (DK24092)
  • National Institute of Diabetes and Digestive and Kidney Diseases (DK 24092)
  • National Center for Research Resources (M0I-RR-01346)
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
beta-cell dysfunction, insulin resistance, impaired glucose tolerance, type 2 diabetes, insulin secretion, insulin sensitivity, oral glucose tolerance test, plasma glucose
MeSH terms
Adult, Blood Glucose, Female, Glucose, Glucose Tolerance Test, Humans, Hyperinsulinism, Insulin, Insulin Resistance, Islets of Langerhans, Liver, Male, Middle Aged, Texas, Glucose Clamp Technique, Glucose Intolerance

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