Prandial glucose effectiveness and fasting gluconeogenesis in insulin-resistant first-degree relatives of patients with type 2 diabetes.
Open accessAbstract
Impaired glucose effectiveness (i.e., a diminished ability of glucose per se to facilitate its own metabolism), increased gluconeogenesis, and endogenous glucose release are, together with insulin resistance and beta-cell abnormalities, established features of type 2 diabetes. To explore aspects of the pathophysiology behind type 2 diabetes, we assessed in a group of healthy people prone to develop type 2 diabetes (n = 23), namely first-degree relatives of type 2 diabetic patients (FDR), 1) endogenous glucose release and fasting gluconeogenesis measured using the 2H2O technique and 2) glucose effectiveness. The FDR group was insulin resistant when compared with an age-, sex-, and BMI-matched control group without a family history of type 2 diabetes (n = 14) (M value, clamp: 6.07 +/- 0.48 vs. 8.06 +/- 0.69 mg x kg(-1) lean body weight (lbw) x min(-1); P = 0.02). Fasting rates of gluconeogenesis (1.28 +/- 0.06 vs. 1.41 +/- 0.07 mg x kg(-1) lbw x min(-1); FDR vs. control subjects, P = 0.18) did not differ in the two groups and accounted for 53 +/- 2 and 60 +/- 3% of total endogenous glucose release. Glucose effectiveness was examined using a combined somatostatin and insulin infusion (0.17 vs. 0.14 mU x kg(-1) x min(-1), FDR vs. control subjects), the latter replacing serum insulin at near baseline levels. In addition, a 360-min labeled glucose infusion was given to simulate a prandial glucose profile. After glucose infusion, the integrated plasma glucose response above baseline (1,817 +/- 94 vs. 1,789 +/- 141 mmol/l per 6 h), the ability of glucose to simulate its own uptake (1.50 +/- 0.13 vs. 1.32 +/- 0.16 ml x kg(-1) lbw x min(-1)), and the ability of glucose per se to suppress endogenous glucose release did not differ between the FDR and control group. In conclusion, in contrast to overt type 2 diabetic patients, healthy people at high risk of developing type 2 diabetes are characterized by normal glucose effectiveness at near-basal insulinemia and normal fasting rates of gluconeogenesis.
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The rise in plasma glucose concentration stimulates insulin secretion, which results in suppression of glucose release and stimulation of glucose uptake.
“The rise in plasma glucose concentration stimulates insulin secretion, which results in suppression of glucose release and stimulation of glucose uptake (12,31).”
From Impaired basal glucose effectiveness but unaltered fasting glucose release and gluconeogenesis during short-term hypercortisolemia in healthy subjects (2004) · cites this paper as [31]
The concurrent rise in concentration of both glucose and insulin will exert a greater response than a rise in either alone.
“The concurrent rise in concentration of both glucose and insulin will exert a greater response than a rise in either alone (31).”
From Impaired basal glucose effectiveness but unaltered fasting glucose release and gluconeogenesis during short-term hypercortisolemia in healthy subjects (2004) · cites this paper as [31]
Cites
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Self-citationContributions of gluconeogenesis to glucose production in the fasted state
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Self-citationContribution of Abnormal Muscle and Liver Glucose Metabolism to Postprandial Hyperglycemia in NIDDM
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“Although knowledge of the mechanisms behind the ability of glucose to promote its own uptake are still only rudimentary, an increase in glucose concentration stimulates translocation of GLUT4 transporters to the plasma membrane in muscle (48), similar to the actions of insulin and contraction on the GLUT4 transporters…”
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Alibegovic, A. C., Højbjerre, L., Sonne, M. P., van Hall, G., Stallknecht, B., Dela, F., & Vaag, A. (2009) · Diabetes · doi:10.2337/db09-0369 · Cited by 103 · see citing works
Nielsen, M. F., Caumo, A., Chandramouli, V., Schumann, W. C., Cobelli, C., Landau, B. R., Vilstrup, H., Rizza, R. A., & Schmitz, O. (2004) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.00566.2002 · Cited by 53 · see citing works
Self-citation
- Authors
- Nielsen, M. F., Nyholm, B., Caumo, A., Chandramouli, V, Schumann, W. C., Cobelli, C., Landau, B. R., Rizza, R. A., & Schmitz, O.
- Affiliations
- Aarhus University Hospital (DK)
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2000-12-01
- Volume
- 49
- Issue
- 12
- Pages
- 2135-2141
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2168624992
- Cited by
- 25
- References
- 6
- Citations by year
- 2018: 1 · 2016: 1 · 2015: 2 · 2014: 1 · 2013: 1 · 2012: 2
- FWCI
- 1.48
- Type
- journal article
- Language
- en
- Open access
- green
- hdl.handle.net
- Licence
- other-oa
- Locations
- Diabetes (publishedVersion)
- PubMed (publishedVersion)
- Archivio Istituzionale della Ricerca (Universita Degli Studi Di Milano) (submittedVersion, other-oa)
- Padua Research Archive (University of Padova) (submittedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (DK 29953)
- 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
- insulin resistance, type 2 diabetes risk, first-degree relatives, glucose uptake, somatostatin, beta-cell function, insulin sensitivity, oral glucose tolerance test, hyperinsulinemic-euglycemic clamp
- MeSH terms
- Adult, Blood Glucose, Diabetes Mellitus, Type 2, Eating, Fasting, Female, Gluconeogenesis, Glucose, Hormones, Humans, Insulin Resistance, Male, Osmolar Concentration, Reference Values, Genetic Predisposition to Disease
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