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Cited by 293Blood Pressure and Hypertension StudiesDiabetes, Cardiovascular Risks, and LipoproteinsHeart Rate Variability and Autonomic Control

The sympathetic response to euglycaemic hyperinsulinaemia: Evidence from microelectrode nerve recordings in healthy subjects

Open access
Berne, C., Fagius, J., Pollare, T., Hjemdahl, P.·1992·Diabetologia
DOI 10.1007/bf00399935
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Abstract

Sympathetic nervous system activation by insulin has been suggested as a mechanism explaining the association between insulin resistance and hypertension. We further examined the effect of insulin by direct microneurographic muscle and skin nerve sympathetic activity recordings during euglycaemic insulin clamps in healthy subjects. The mean plasma insulin level was elevated from 5.3 +/- 0.7 to 92.2 +/- 2.2 mU/l in seven subjects during a 90-min one-step clamp. In six other subjects plasma insulin was further raised from 85.7 +/- 4.0 mU/l to 747 +/- 53 mU/l between 45-90 min (two-step clamp). Four of the latter subjects received a sham clamp with NaCl infusions only on a second recording session. At the low dose of insulin muscle nerve sympathetic activity increased from a resting level of 22.7 +/- 5.0 bursts per min to 27.7 +/- 5.0 bursts per min at 15 min (p less than 0.05). The increases in muscle nerve sympathetic activity were significant (p less than 0.001; ANOVA) throughout insulin infusion, with a slight further increase (from 29.2 +/- 1.6 to 32.3 +/- 1.9 bursts per min) at the supraphysiological insulin concentration. During sham clamps muscle nerve sympathetic activity did not increase. Both insulin clamps induced minor, but significant, increases in forearm venous plasma noradrenaline concentrations. Skin nerve sympathetic activity (n = 3) did not change during insulin infusions. Heart rate increased slightly but significantly (p less than 0.005), during the insulin clamps. Blood pressure was not notably affected. In conclusion, hyperinsulinaemia was associated with increased vasoconstrictor nerve activity to skeletal muscle and with no change of sympathetic outflow to skin.

AI snapshot

Written from the paper’s full text.

TL;DR

In healthy subjects, euglycaemic hyperinsulinaemia increased muscle sympathetic vasoconstrictor nerve activity without changing skin sympathetic activity, while blood pressure was largely unaffected. The response occurred at high physiological insulin and increased further at supraphysiological levels, with only minor rises in plasma noradrenaline and heart rate.

Key findings

  • Muscle nerve sympathetic activity (MSA) rose during one-step insulin clamp from 22.7 ± 5.0 bursts/min at rest to 27.7 ± 5.0 at 15 min (p < 0.05), with a maximum of 29.0 ± 4.6 at 30 min (p < 0.001; ANOVA), and remained elevated at 26.9 ± 3.6 at 90 min.
  • During two-step clamp, MSA increased from 22.1 ± 2.7 to 29.2 ± 1.6 bursts/min at the lower insulin level and further to 32.3 ± 1.9 at 90 min (p < 0.0001; ANOVA); sham NaCl infusions produced no MSA increase.
  • Skin nerve sympathetic activity (n = 3) did not change during insulin infusions.
  • Plasma noradrenaline increased slightly but significantly during both clamps (one-step p < 0.05; two-step p < 0.01), while sham remained stable; heart rate increased slightly and significantly (one-step p < 0.0001; two-step p < 0.005), and blood pressure was not notably affected except a late systolic rise from 127.7 to 133.5 mmHg at 90 min during high-dose insulin.

Methods

  • Sixteen non-obese healthy volunteers (10 men, 6 women; mean age 29 years, range 22–44; mean BMI 21.8, range 18.8–24.6 kg/m²) underwent 20 microneurography registrations.
  • Euglycaemic insulin clamps were performed: one-step infusion at 56 mU·m⁻²·min⁻¹ for 90 min in ten experiments (7 MSA, 3 SSA); two-step infusion from 56 to 312 mU·m⁻²·min⁻¹ between 45–90 min in six MSA experiments; four subjects also received sham NaCl clamps. Plasma insulin rose from 5.3 ± 0.7 to 92.2 ± 2.2 mU/l in one-step clamps and from 85.7 ± 4.0 to 747 ± 53 mU/l in two-step clamps.
  • Peroneal nerve microneurography recorded MSA or SSA; bursts were counted over 6-min periods at −15, 0, 15, 30, 45, 60, 75, and 90 min, with ANOVA and Dunnett’s t-test for MSA and inspection only for SSA.

Limitations

  • The paper states that blood pressure was measured only intermittently (3-min intervals), so minor fluctuations may have escaped detection; it also states that the exact role of insulin-induced central neuromodulation is largely unknown and whether insulin sympathetic stimulation contributes to hypertension remains an open question.
  • SSA findings are based on n = 3 and were analyzed by inspection only; sham clamps were performed in four subjects, and the study was acute in healthy non-obese volunteers, limiting generalizability to insulin-resistant or hypertensive populations (evident from the text).
  • The study cannot distinguish direct central sympathetic stimulation from a baroreflex-mediated response; the authors discuss both possibilities and note no clear fall in blood pressure, but the mechanism remains unresolved (stated and evident).

Model-written summary. Check it against the paper before relying on it.

Integrity signals

Registry

Crossref · 10.1007/bf00399935

Cites

46 of 46 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Claims the paper makes

0 of 50 cited sources checked · 0 supported · 0 flagged

  • Findingown data

    During the one-step euglycaemic insulin clamp, mean plasma insulin was elevated to 92.2 ± 2.2 mU/l (15-90 min).

    “The one-step clamp, with a constant insulin infusion rate during MSA recordings, resulted in a mean plasma insulin level of 92.2 _+ 2.2 mU/1 (15-90 min) (Fig. 1A).”
    Quote in the paperSubstantial claim
  • Findingown data

    In the four subjects who also received sham clamps, MSA remained at the resting level throughout the experiment when 0.9% NaCl was infused.

    “In the four subjects who also received sham clamps, ~ 60 MSA remained at the resting level throughout the experiment when 0.9 % NaC1 was infused (Fig. 2 C).”
    Quote in the paperNot a substantial claim
  • Findingown data

    During the two-step clamp, a further increase of plasma insulin to supraphysiological concentration was accompanied by a slight further increase in MSA from 29.2 ± 1.6 to 32.3 ± 1.9 bursts/min.

    “The increases in muscle nerve sympathetic activity were significant (p < 0.001; ANOVA) throughout insulin infusion, with a slight further increase (from 29.2 + 1.6 to 32.3 + 1.9 bursts per min) at the supraphysiological insulin concentration.”
    Quote in the paperSubstantial claim
    • Rests on an assumption: The high-dose plasma insulin level achieved (747 mU/l) is supraphysiological.
  • Findingown data

    The increase in MSA was less prominent in the present study than that observed following the oral glucose load (maximal increase 17.4 ± 4.4 bursts/min after oral glucose vs 6.3 ± 0.4 bursts/min in the seven subjects given the low dose of insulin; p = 0.025, t-test of non-paired observations).

    “The increase in MSA was less prominent in the present study than that observed following the oral glucose load [12] -maximal increase was 17.4 + 4.4 bursts per rain after oral glucose intake and 6.3 + 0.4 bursts per rain in the seven subjects given the low dose of insulin in the present study (p = 0.025, t-test of non-paired observations).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [12] Berne C, Fagius J, Niklasson F (1989) Sympathetic response to oral carbohydrate administration. Evidence from microelectrode nerve recordings. J Clin Invest 84: 1403?1409 source

      Not checked in the free run.

  • Findingown data

    During sham experiments, plasma insulin remained at the fasting level (mean 7.6 mU/l, range 6.5-8.7 mU/l).

    “During the sham experiments plasma insulin remained at the fasting level of 7.6 mU/1 (range 6.5-8.7 mU/1).”
    Quote in the paperSubstantial claim
  • May combine two claims. 14
  • Classified as probably not a substantial claim. 7
  • The quote only partly states this claim. 2

  • May combine two claims.

    Findingown data

    During the two-step euglycaemic insulin clamp, mean plasma insulin was 85.7 ± 4.0 mU/l during low-dose infusion and 747 ± 53 mU/l during high-dose infusion.

    “During the twostep clamp the mean insulin level was 85.7 + 4.0 mUff during the low-dose infusion and 747 + 53 mU/1 during the high-dose infusion (Fig. lB).”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Findingown data

    During the two-step clamp, haematocrit decreased from 42.0% to 40.8 ± 1.1% (p < 0.001; ANOVA).

    “The corresponding values for the two-step clamp were 42.0• and 40.8+1.1% (p <0.001; ANOVA), respectively.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Findingown data

    During the one-step clamp, haematocrit decreased from 38.0 ± 1.4% to 37.6 ± 1.2% after 90 min (p < 0.01; ANOVA).

    “During the one-step clamp haematocrit decreased from 38.0+1.4% to 37.6+1.2%after 90min (p <0.01; ANOVA).”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingown data

    During the one-step clamp, there were no significant changes in systolic or diastolic blood pressure.

    “During the one-step clamp there were no significant changes in systolic or diastolic blood pressure (Fig. 6 A).”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingown data

    In the sham clamp, plasma noradrenaline remained stable, with no significant changes over time.

    “In the sham clamp plasma noradrenaline remained stable, with no significant changes over time (1.39+0.51nmol/1at 0min and 1.65 + 0.41 nmol/1 at 90 min).”
    Quote in the paperNot a substantial claim

  • The quote only partly states this claim.

    Findingown data

    During the one-step clamp, MSA increased from a resting level of 22.7 ± 5.0 bursts/min to 27.7 ± 5.0 bursts/min at 15 min (p < 0.05).

    “During the one-step clamp (Fig. 2 A), the elevation of plasma insulin was rapidly followed by an increase in MSA from a resting level of 22.7 + 5.0 bursts per min to 27.7 + 5.0 bursts per rain (at 15 min) with a maximum of 29.0 + 4.6 bursts per min at 30 min (p < 0.001; ANOVA).”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Premiseown data

    There is a significant association between MSA and serum insulin concentrations after glucose ingestion, suggesting that insulin per se may, at least partly, mediate this response.

    “There was also a significant association between MSA and serum insulin concentrations after glucose ingestion, which suggested that insulin per se may, at least partly, mediate this response.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [12] Berne C, Fagius J, Niklasson F (1989) Sympathetic response to oral carbohydrate administration. Evidence from microelectrode nerve recordings. J Clin Invest 84: 1403?1409 source

      Not checked in the free run.

  • Classified as probably not a substantial claim.

    Premisecitation

    Acute studies have suggested that euglycaemic elevation of plasma insulin increases sympathetic nervous system activity.

    “Acute studies have suggested that euglycaemic elevation of plasma insulin increases sympathetic nervous system activity [6,7].”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [6] Rowe JW, Young JB, Minaker KL, Stevens AL, Pallotta J, Landsberg L (1981) Effect of insulin and glucose infusions on sympathetic nervous system activity in normal man. Diabetes 30: 219?255 source

      Not checked in the free run.

    • cites [7] O'Hare JA, Minaker KL, Meneilly GS, Rowe JW, Pallotta JA, Young JB (1989) Effect of insulin on plasma norepinephrine and 3,4 dihydroxyphenylalanine in obese men. Metabolism 38: 322?329 source

      Not checked in the free run.

  • Classified as probably not a substantial claim.

    Study design and conductcitation

    The criteria for the sympathetic origin of the recorded nerve signal have been summarized previously.

    “The criteria for the sympathetic origin of the signal recorded have been summarized previously [11].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [11] Wallin BG, Fagius J (1988) Peripheral sympathetic neural activity in conscious humans. Ann Rev Physiol 50: 565?756 source

      Not checked in the free run.

  • May combine two claims. The quote only partly states this claim.

    Study design and conductcitation

    Sham clamps with NaCl infusions were performed to exclude an effect of the experimental situation and of volume receptor unloading on MSA.

    “There were two major reasons to perform sham clamps in order to substantiate the observation of a response of MSA to insulin.First, even if MSA is weakly sensitive to environmental stress [20] such an effect caused by the experimental situation had to be excluded.Secondly, MSA may also increase in response to unloading of volume receptors [21].”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [20] Hjemdahl P, Fagius J, Freyschuss U et al. (1989) Muscle sympathetic activity and norepinephrine release during mental challenge in humans. Am J Physiol 257: E654-E664

      Not checked in the free run.

    • cites [21] Sundlöf G, Wallin BG (1978) Effect of lower body negative pressure on human muscle nerve sympathetic activity. J Physiol 278: 525?532 source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Skin nerve sympathetic activity (SSA), involved in body temperature homeostasis and not under baroreceptor influence, was not changed by glucose intake.

    “Skin nerve sympathetic activity (SSA), involved in body temperature homeostasis and not under baroreceptor influence [11], was not changed by glucose intake [121.”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [11] Wallin BG, Fagius J (1988) Peripheral sympathetic neural activity in conscious humans. Ann Rev Physiol 50: 565?756 source

      Not checked in the free run.

    • cites [12] Berne C, Fagius J, Niklasson F (1989) Sympathetic response to oral carbohydrate administration. Evidence from microelectrode nerve recordings. J Clin Invest 84: 1403?1409 source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    The sympathetic nervous system is complex and composed of many functionally different subdivisions, which are not necessarily activated simultaneously.

    “However, the sympathetic nervous system is complex and is composed of many functionally different subdivisions, which are not necessarily activated simultaneously [9].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [9] Hjemdahl P (1990) Physiology of the autonomic nervous system as related to cardiovascular function: implications for stress research. In: Byrne DG, Rosenman RH (eds) Anxiety and the heart. Hemisphere, New York, pp 95?157

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Study design and conductcitation

    The plasma catecholamine method is well validated and has inter- and intra-assay coefficients of variation of 2-3% in the nanomolar range.

    “The method is well validated and has inter-and intra-assay coefficients of variation of 2-3 % in the nanomolar range [19].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [19] Hjemdahl P (1987) Catecholamine measurements by high-performance liquid chromatography with electrochemical detection. Methods Enzymol 142: 521?534 source

      Not checked in the free run.

  • May combine two claims.

    Study design and conductcitation

    The target plasma glucose during the clamp was kept slightly above fasting to avoid hypoglycaemia, which would have increased MSA and SSA.

    “The target level for plasma glucose during the clamp was slightly above the fasting level, since it was important to avoid hypoglycaemia, which would have increased MSA and SSA [17,18].”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [17] Fagius J, Niklasson F, Berne C (1986) Sympathetic outflow in human muscle nerves increases during hypoglycemia. Diabetes 35: 1124?1129 source

      Not checked in the free run.

    • cites [18] Berne C, Fagius J (1986) Skin nerve sympathetic activity during insulin-induced hypoglycaemia. Diabetologia 29: 855?860 source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductown data

    Plasma catecholamine analyses were performed without knowledge of the results from the nerve recordings.

    “The analyses were performed without knowledge of the results from the nerve recordings.”
    Quote in the paperNot a substantial claim

  • Classified as probably not a substantial claim.

    Study design and conductown data

    In the sham clamps, the subjects were not informed of the substitution of insulin and glucose infusions by 0.9% NaCl.

    “The subjects were not informed of this substitution.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Premisecitation

    Insulin receptors are widely distributed in the brain and are primarily located on neurons.

    “Insulin receptors are widely distributed in the brain, and are primarily located on neurons [45,46].”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [45] Heidenreich KA (1991) Insulin in the brain. What is its role. TEM 2: 9?12

      Not checked in the free run.

    • cites [46] Hill JM, Lesniak MA, Pert CB, Roth J (1986) Autoradiographic localization of insulin receptors in rat brain: prominence in olfactory and limbic areas. Neuroscience 17: 1127?1131 source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Studies with the euglycaemic clamp have yielded conflicting results in humans regarding blood flow: some reported increased blood flow in skeletal muscles of the limbs, whereas others reported unchanged blood flow.

    “Studies with the euglycaemic clamp have yielded conflicting results in humans.A number of studies have reported an increased blood flow in skeletal muscles of the limbs [14,26,[34][35][36], whereas others have reported unchanged blood flow [37][38][39].”
    Quote in the paperNot a substantial claim0 of 8 sources checked
    • cites [14] Anderson EA, Hoffmann RP, Balon TW, Sinkey CA, Mark AL (1991) Hyperinsulinaemia produces both sympathetic neural activation and vasodilation in normal human beings. J Clin Invest 87: 2246?2252 source

      Not checked in the free run.

    • cites [26] Scott AR, Bennett T, MacDonald IA (1988) Effects of hyperinsulinaemia on the cardiovascular responses to graded hypovolemia in normal and diabetic subjects. Clin Sci 75: 85?92 source

      Not checked in the free run.

    • cites [34] Creager MA, Liang C-S, Coffman JD (1985) Beta adrenergicmediated vasodilator response to insulin in the human forearm. J Pharmacol Exp Therapeut 235: 709?714

      Not checked in the free run.

    • cites [35] Richter EA, Mikines KJ, Galbo H, Kiens B (1989) Effects of exercise on insulin action in human skeletal muscle. J Appl Physiol 66: 876?885 source

      Not checked in the free run.

    • cites [36] Laakso M, Edelman SV, Brechtel G, Baron AD (1990) Decreased effect of insulin to stimulate skeletal muscle blood flow in obese man. J Clin Invest 85: 1844?1852 source

      Not checked in the free run.

    • cites [37] James DE, Burleigh KM, Storlien LH, Bennett SP, Kraegen EW (1986) Heterogeneity of insulin action in muscle: influence of blood flow. Am J Physiol 251: E422-E430

      Not checked in the free run.

    • cites [38] Jackson RA, Hamling JB, Blix PM et al. (1986) The influence of graded hyperglycemia with and without physiological hyperinsulinaemia on forearm glucose uptake and other metabolic responses in man. J Clin Endocr Metab 63: 594?604 source

      Not checked in the free run.

    • cites [39] Yki-Järvinen H, Young AA, Lamkin C, Foley JE (1987) Kinetics of glucose disposal in whole body and across the forearm. J Clin Invest 79: 1713?1719 source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Insulin has been shown to cause vasodilation and to attenuate noradrenaline- and angiotensin II-induced vasoconstriction in vitro.

    “Insulin has been shown to cause vasodilation [32] and attenuates noradrenaline-and angiotensin II-induced vasoconstriction in vitro [33].”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [32] Liang CS, Doherty JU, Faillace R et al. (1982) Insulin infusion in conscious dogs. Effects on systemic and coronary hemodynamics, regional blood flows, and plasma catecholamines. J Clin Invest 69: 1321?1336 source

      Not checked in the free run.

    • cites [33] Yagi S, Takata S, Kiyokawa H et al. (1988) Effects of insulin on vasoconstrictive responses to norepinephrine and angiotensin II in rabbit femoral artery and vein. Diabetes 37: 1064?1067 source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Insulin has been shown to alter the neuronal firing rate and interfere with catecholamine uptake in cultured neurons.

    “Insulin has also been shown to alter the neuronal firing rate [47] and interfere with catecholamine uptake in cultured neurons [48], but the exact role for insulin-induced central neuromodulation of the sympathetic nervous system activity is largely unknown.”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [47] Sakaguchi T, Takahashi M, Bray GA (1988) Diurnal changes in sympathetic activity. Relation to food intake and to insulin injected into the ventromedial or suprachiasmatic nucleus. J Clin Invest 82: 282?286 source

      Not checked in the free run.

    • cites [48] Boyd FT, Clarke DW, Raizada MK (1985) Insulin receptors and insulin modulation of norepinephrine uptake in neuronal cultures from rat brain. J Biol Chem 260: 15880?15884 source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    A dose-response relationship between plasma insulin concentration and enhanced leg blood flow has been established, and insulin resistance is associated with a blunted vasodilatory response.

    “Recently, a dose-response relationship between the plasma insulin concentration and enhanced leg blood flow has been established and insulin resistance was associated with a blunted vasodilatory response [36].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [36] Laakso M, Edelman SV, Brechtel G, Baron AD (1990) Decreased effect of insulin to stimulate skeletal muscle blood flow in obese man. J Clin Invest 85: 1844?1852 source

      Not checked in the free run.

21 of 21

  • The paper relies on this without support.

    The low-dose plasma insulin level achieved (about 86-92 mU/l) is in the high physiological range.

    “The plasma insulin concentration attained during the low dose of insulin was in the high physiological range, whereas the high dose of insulin resulted in a supraphysiological plasma insulin concentration.”

  • The paper relies on this without support.

    The high-dose plasma insulin level achieved (747 mU/l) is supraphysiological.

    “The plasma insulin concentration attained during the low dose of insulin was in the high physiological range, whereas the high dose of insulin resulted in a supraphysiological plasma insulin concentration.”
2 of 2

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • In humans, acute euglycemic hyperinsulinemia stimulates both sympathetic efferent activity and blood flow in skeletal muscle.

    “Euglycemic hyperinsulinemia evokes both sympathetic activation and vasodilation in skeletal muscle, but the mechanism remains unknown.”

    From Differential effects of hyperinsulinemia and carbohydrate metabolism on sympathetic nerve activity and muscle blood flow in humans (1993) · cites this paper as [7]

    The Discussion reports that euglycaemic hyperinsulinaemia increased sympathetic nerve activity to skeletal muscle in healthy humans. It also describes another study finding concomitant arm vasodilation and leaves the mechanism of sympathetic activation unresolved. However, it says human clamp studies found conflicting blood-flow results, so the unqualified claim that hyperinsulinaemia evokes skeletal-muscle vasodilation overstates the evidence it presents. (LLM, conf=0.84)

    Experimental — accuracy not yet measured

  • A balance between insulin's opposing sympathoexcitatory pressor and vasodilatory depressor effects may explain that in lean healthy subjects acute hyperinsulinemia at high physiologic concentrations does not raise arterial pressure.

    “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 [7]

Cites

Flagged first, then by citations

Research works printed but not linked: 2

  1. Hjemdahl P (1990) Physiology of the autonomic nervous system as related to cardiovascular function: implications for stress research. In: Byrne DG, Rosenman RH (eds) Anxiety and the heart. Hemisphere, New York, pp 95?157
  2. Berne C, Pollare T, Fagius J (1989) The sympathetic outflow in vasoconstrictor nerve fascicles to muscle is increased during euglycaemic hyperinsulinaemia. Diabetologia 32: 465A (Abstract)

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Authors
Berne, C., Fagius, J., Pollare, T., & Hjemdahl, P.
Affiliations
  • Uppsala University Hospital (SE)
  • Uppsala University (SE)
  • Karolinska University Hospital (SE)
ORCID
Venue
Diabetologia
Publisher
Springer Science and Business Media LLC
Published
1992-09
Volume
35
Issue
9
Pages
873-879
ISSN
  • 0012-186X (ISSN-L)
  • 1432-0428
DOI
10.1007/bf00399935
OpenAlex
W2316480407
Semantic Scholar
9b8e1202d333ed3105d057bc78bed748006e2d06
Cited by
293
References
46
Citations by year
2026: 1 · 2025: 1 · 2024: 1 · 2023: 3 · 2022: 3 · 2021: 3 · 2020: 3 · 2019: 5 · 2018: 4 · 2017: 4 · 2016: 4 · 2015: 9 · 2014: 11 · 2013: 10 · 2012: 11
FWCI
10.25
Type
journal article
Language
en
Open access
Licence
www.springer.com/tdm (tdm)
Locations
  • Diabetologia (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Novo Nordisk
  • Novo Nordisk Pharma
  • Medical Research Council
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Blood Pressure and Hypertension Studies
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Heart Rate Variability and Autonomic Control
Keywords
insulin, hyperinsulinemia, sympathetic nervous system, norepinephrine, vasoconstriction, insulin resistance, hypertension, heart rate
MeSH terms
Adult, Analysis of Variance, Blood Glucose, Blood Pressure, Electrodes, Implanted, Female, Humans, Hyperinsulinism, Insulin, Insulin Resistance, Male, Microelectrodes, Muscles, Pressoreceptors, Reference Values, Skin, Sympathetic Nervous System, Vasoconstriction, Glucose Clamp Technique

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