Increased nonoxidative glucose metabolism in idiopathic reactive hypoglycemia
Abstract
Idiopathic reactive hypoglycemia (IRH) is responsible for postprandial hypoglycemia. Normal insulin secretion and reduced response of glucagon to acute hypoglycemia, but mostly increased insulin sensitivity, represent the metabolic features of this syndrome- The present study has two aims: first, to investigate the fate of glucose utilization inside the cells to assess whether increased glucose disposal in IRH is due to the oxidative and/or nonoxidative pathway; and second, to evaluate glucagon response to prolonged insulin-induced hypoglycemia. In eight patients with IRH and eight normal (N) subjects, we performed two studies on different days: (1) 120-minute euglycemic-hyperinsulinemic (1.0 mU . kg-1 . min-1 regular human insulin) clamp associated with indirect calorimetry; and (2) 180-minute hypoglycemic (2.22 to 2.49 mmo/L achieved through 0.85 mU . kg-1 . min-1 intravenous [IV] regular human insulin) clamp. The results showed an increased insulin-mediated glucose uptake in IRH (9.10 +/- 0.19 v 6.78 +/- 0.18 mg kg-1 . min-1, P < .005). Glucose oxidation was similar in IRH subjects and controls both in basal conditions (1.39 +/- 0.16 v 1.42 +/- 0.15 mg . kg-1 . min-1 and during the clamp studies (2.57 +/- 0.21 v 2.78 +/- 0.26 mg . kg-1 . min-1. In contrast, nonoxidative glucose disposal was significantly higher in IRH than in N subjects (6.53 +/- 0.30 v 4.00 +/- 0.21 mg . kg-1 . min-1, P < .001). During insulinization, fat oxidation was reduced slightly more in IRH than in control subjects. During the hypoglycemic clamp, a significant (P < .01) increase in plasma glucagon concentrations was observed in normal subjects as compared with baseline, whereas no change occurred in IRH patients. In conclusion, in IRH: (1) increased insulin-mediated glucose disposal is due to the increase of nonoxidative glucose metabolism; and (2) glucagon secretion has been confirmed to be inadequate. The increase of insulin sensitivity associated with a deficiency in glucagon secretion can widely explain the occurrence of hypoglycemia in the late postprandial phase.
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Idiopathic RH may arise from high insulin sensitivity, probably most frequently (50-70%), which is not measured by indices of insulin sensitivity.
“RH may arise from an increased insulin response, which might be related either to insulin resistance or to increased GLP-1, renal glycosuria, defects in glucagon response, or high insulin sensitivity probably the most frequently (50–70%), which is not be measured by indices of insulin sensitivity.[5]”
From Postprandial Reactive Hypoglycemia (2019) · cites this paper as [5]
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“RH may arise from an increased insulin response, which might be related either to insulin resistance or to increased GLP-1, renal glycosuria, defects in glucagon response, or high insulin sensitivity probably the most frequently (50–70%), which is not be measured by indices of insulin sensitivity.[5] Earliest changes…”
BackgroundDefining and Characterizing Postprandial Reactive Hypoglycemia
Sweatt, S. K., Thomas, D. M., LaPorte, G. J., Chauff, S., Stefanovski, D., & Gower, B. A. (2026) · Nutrients · doi:10.3390/nu18050822 · Cited by 2 · see citing works
- Authors
- Leonetti, F., Foniciello, M., Iozzo, P., Riggio, O., Merli, M., Giovannetti, P., Sbraccia, P., Giaccari, A., & Tamburrano, G.
- Affiliations
- Sapienza University of Rome (IT)
- Venue
- Metabolism
- Publisher
- Elsevier BV
- Published
- 1996-05
- Volume
- 45
- Issue
- 5
- Pages
- 606-610
- ISSN
- 0026-0495 (ISSN-L)
- OpenAlex
- W2020146245
- Semantic Scholar
- 81f8910fb696ec5409349645988dc6c48db4df05
- Cited by
- 26
- References
- 33
- Citations by year
- 2026: 2 · 2024: 3 · 2021: 1 · 2019: 2 · 2016: 3 · 2015: 2 · 2013: 1
- FWCI
- 0.00
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Metabolism (publishedVersion)
- PubMed (publishedVersion)
- IRIS Research product catalog (Sapienza University of Rome) (submittedVersion)
- Topics
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Management and Research
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Keywords
- nonoxidative glucose metabolism, glucose oxidation, insulin sensitivity, insulin-stimulated glucose uptake, glucagon secretion, insulin-induced hypoglycemia, fat oxidation, postprandial hypoglycemia, hyperinsulinemic-euglycemic clamp, hypoglycemic clamp, glucose disposal, insulin resistance, glucose-6-phosphate
- MeSH terms
- Adult, Blood Glucose, Humans, Hypoglycemia, Insulin, Oxidation-Reduction
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