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Cited by 753Diabetes Management and ResearchDiabetes, Cardiovascular Risks, and LipoproteinsPancreatic function and diabetes

Measurement of Plasma Glucose, Free Fatty Acid, Lactate, and Insulin for 24 h in Patients With NIDDM

Reaven, Gerald M, Hollenbeck, Clarie, Jeng, Chii-Yang, Wu, Min Shung, Chen, Yii-Der Ida·1988·Diabetes
DOI 10.2337/diab.37.8.1020
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Abstract

Fasting and postprandial plasma glucose, free fatty acid (FFA), lactate, and insulin concentrations were measured at hourly intervals for 24 h in 27 nonobese individuals—9 with normal glucose tolerance, 9 with mild non-insulin-dependent diabetes mellitus (NIDDM, fasting plasma glucose < 175 mg/dl), and 9 with severe NIDDM (fasting plasma glucose > 250 mg/dl). In addition, hepatic glucose production (HGP) was measured from midnight to 0800 in normal individuals and patients with severe NIDDM. Plasma glucose concentration was highest in patients with severe NIDDM, lowest in those with normal glucose tolerance, and intermediate in those with mild NIDDM (two-way ANOVA, P < .001). Variations in plasma FFA and lactate levels of the three groups were qualitatively similar, with lowest concentrations seen in normal individuals, intermediate levels in the group with mild NIDDM, and the highest concentration in those with severe NIDDM (two-way ANOVA, P < .001). Of particular interest was the observation that plasma FFA concentrations were dramatically elevated from midnight to 0800 in patients with severe NIDDM. The 24-h insulin response was significantly increased in patients with mild NIDDM, with comparable values seen in the other two groups. Values for HGP fell progressively throughout the night in normal individuals and patients with severe NIDDM, despite a concomitant decline in plasma glucose and insulin levels. Although the magnitude of the fall in HGP was greater in NIDDM, the absolute value was significantly (P < .001) greater than normal throughout the period of observation. These results demonstrate that there are differences in substrate level between individuals with normal glucose tolerance and patients with NIDDM and differing degrees of glucose intolerance, unrelated to ambient insulin level, and these changes persist over 24 h.

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  • The metabolic derangements of Type 2 diabetes include an increase in plasma NEFA concentrations, which produce deleterious effects on insulin-sensitive tissues and the beta cell.

    “The metabolic derangements of Type 2 diabetes include an increase in plasma NEFA concentrations [145], which has been shown to produce deleterious effects on the insulin-sensitive tissues and the beta cell.”

    From The relative contributions of insulin resistance and beta-cell dysfunction to the pathophysiology of type 2 diabetes (2003) · cites this paper as [145]

  • Non-diabetic obese and type 2 diabetic individuals have day-long elevation of plasma free fatty acid concentration that fails to suppress normally after a mixed meal or oral glucose load.

    “Nondiabetic obese and type 2 diabetic individuals are characterized by day-long elevation in the plasma FFA concentration, which fails to suppress normally after ingestion of a mixed meal or an oral glucose load [60].”

    From Pathogenesis of insulin resistance in skeletal muscle (2010) · cites this paper as [60]

  • Increased hepatic de novo lipogenesis precedes the development of adipose tissue insulin resistance, which subsequently leads to increased flux of fatty acids to the liver.

    “these results suggest that increased hepatic de novo lipogenesis precede the development of adipose tissue insulin resistance, which subsequently leads to increased flux of fatty acids to the liver (16, 17).”

    From The role of skeletal muscle insulin resistance in the pathogenesis of the metabolic syndrome (2007) · cites this paper as [17]

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Authors
Reaven, G. M., Hollenbeck, C., Jeng, C.-Y., Wu, M. S., & Chen, Y.-D. I.
Affiliations
VA Palo Alto Health Care System (US)
ORCID
Chen, Yii-Der Ida
Venue
Diabetes
Publisher
American Diabetes Association
Published
1988-08-01
Volume
37
Issue
8
Pages
1020-1024
ISSN
  • 0012-1797 (ISSN-L)
  • 1939-327X
DOI
10.2337/diab.37.8.1020
OpenAlex
W2109820048
Cited by
753
References
0
Citations by year
2026: 3 · 2025: 6 · 2024: 13 · 2023: 13 · 2022: 6 · 2021: 21 · 2020: 27 · 2019: 22 · 2018: 25 · 2017: 32 · 2016: 27 · 2015: 28 · 2014: 37 · 2013: 34 · 2012: 27
FWCI
4.05
Type
journal article
Language
en
Open access
closed
Locations
  • Diabetes (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health
  • National Institute of Diabetes and Digestive and Kidney Diseases (DK30732)
  • National Center for Research Resources (RR-00070-26)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Management and Research
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
Keywords
type 2 diabetes, plasma glucose, free fatty acids, lactate, insulin response, hepatic glucose production, circadian variation, fasting blood glucose, postprandial blood glucose, glucose tolerance
MeSH terms
Blood Glucose, Circadian Rhythm, Diabetes Mellitus, Type 2, Fatty Acids, Nonesterified, Humans, Insulin, Lactates, Monitoring, Physiologic, Time Factors

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