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Effect of Insulin and Glucose Infusions on Sympathetic Nervous System Activity in Normal Man
Abstract
Recent studies indicate a link between carbohydrate intake and the functional state of the sympathetic nervous system. Fasting or carbohydrate restriction decreases sympathetic activity, while glucose ingestion or dietary supplementation with sucrose increases sympathetic nerve activity. To examine the potential contributions of hyperglycemia and hyperinsulinemia to sympathetic stimulation, sympathetic activity was assessed by measurement of plasma norepinephrine (NE) levels and concomitant cardiovascular indices in nonobese young men during glucose and insulin infusions using glucose clamp techniques. In the insulin infusion studies (euglycemic glucose clamp), insulin was administered at 2 mU/kg/min and 5 mU/kg/min for 2 h while blood glucose was maintained at basal levels by a variable rate of glucose infusion. In the hyperglycemic studies, blood glucose was raised 125 mg/dl above basal and maintained at that level for 2h. In response to both insulin infusions, plasma NE rose progressively over the course of the study, increasing 50% with the 2-mU infusion (from mean basal value of 240 ± 34 pg/ml to 360 ± 41 at 150 min, P < 0.001 for changes over time by analysis of variance) and 117% with the 5-mil infusion (from 254 ± 20 pg/ml to 551 ± 88 at 150 min, P < 0.001). The plasma NE response was greater with the 5-mll than with the 2-mU insulin infusion (P < 0.001), and similarly, was greater during the 2-mU insulin infusion than during a control test in which neither insulin nor glucose was infused (P < 0.001). Associated with the elevations in plasma NE In the 2-mU insulin infusion were increases in pulse rate (P < 0.05), pulse pressure (P < 0.005), and pulse rate - systolic blood pressure product (P < 0.01), and during the 5-mU insulin infusions there were increases in pulse pressure (P < 0.001), mean arterial blood pressure (P < 0.001), and pulse rate - systolic blood pressure product (P < 0.001). Plasma NE did not change during the hyperglycemic glucose clamp nor during control tests, and pulse pressure in the hyperglycemic studies (P < 0.005) was the only cardiovascular measurement increased by these two infusion protocols. The clearance of NE in three subjects was unaffected by the 2-mU insulin infusion. Thus, insulin infusion increases sympathetic nervous system activity in the absence of changes in blood glucose.
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In the citing paper
“In the present study, infusion of exogenous glucose in amounts comparable to those used in this earlier study (26) also did not increase plasma norepinephrine levels significantly, but evoked highly significant increases in sympathetic discharge targeted at skeletal muscle.”
From Differential effects of hyperinsulinemia and carbohydrate metabolism on sympathetic nerve activity and muscle blood flow in humans (1993) · cites this paper as [26]
In the citing paper
“However, the conclusions of one study were based upon the absence of a detectable effect of glucose infusion on plasma norepinephrine levels (5, 26), a relatively insensitive index of sympathetic discharge (34–36).”
From Differential effects of hyperinsulinemia and carbohydrate metabolism on sympathetic nerve activity and muscle blood flow in humans (1993) · cites this paper as [26]
In the citing paper
“Second, a balance between insulin's opposing sympathoexcitatory pressor and vasodilatory depressor effects may offer a potential explanation for the present, and earlier (6, 7, 26) observations, that in lean healthy subjects acute hyperinsulinemia at high physiologic concentrations does not raise arterial pressure.”
From Differential effects of hyperinsulinemia and carbohydrate metabolism on sympathetic nerve activity and muscle blood flow in humans (1993) · cites this paper as [26]
In the citing paper
“Since insulin stimulates the sympathetic nervous system (SNS), 16,17 and since obese patients have increased SNS activity, [18][19][20] a role for insulin-mediated SNS stimulation seems a likely factor in the pathogenesis of high BP in the setting of central obesity.”
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Background
Metadata
- Authors
- Rowe, J. W., Young, J. B., Minaker, K. L., Stevens, A. L., Pallotta, J., & Landsberg, L.
- Affiliations
- Harvard University (US)
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 1981-03-01
- Volume
- 30
- Issue
- 3
- Pages
- 219-225
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2111038792
- Cited by
- 1,143
- References
- 0
- Citations by year
- 2026: 2 · 2025: 7 · 2024: 5 · 2023: 15 · 2022: 8 · 2021: 8 · 2020: 9 · 2019: 13 · 2018: 15 · 2017: 20 · 2016: 19 · 2015: 13 · 2014: 19 · 2013: 15 · 2012: 14
- FWCI
- 23.06
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Diabetes (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Institute on Aging
- 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 › Endocrinology, Diabetes and Metabolism › Diet, Metabolism, and Disease
- Keywords
- insulin, glucose infusion, sympathetic activity, plasma norepinephrine, hyperinsulinemia, hyperglycemia, hyperinsulinemic-euglycemic clamp, pulse pressure, blood pressure, heart rate, carbohydrate metabolism, young men, dietary sucrose
- MeSH terms
- Adolescent, Adult, Blood Glucose, Blood Pressure, Glucose, Humans, Insulin, Kinetics, Male, Norepinephrine, Pulse, Sympathetic Nervous System
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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