The DOI matches its Crossref record.
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.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
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 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.”
Citations
Cited by
Sorted by citations
Role of Insulin Resistance in Human Disease
Reaven, G. M. (1988) · Diabetes · doi:10.2337/diab.37.12.1595 · Cited by 12,154
Nanozymes: Classification, Catalytic Mechanisms, Activity Regulation, and Applications
Huang, Y., Ren, J., & Qu, X. (2019) · Chemical Reviews · doi:10.1021/acs.chemrev.8b00672 · Cited by 3,581
Insulin Resistance in Essential Hypertension
Ferrannini, E., Buzzigoli, G., Bonadonna, R., Giorico, M. A., Oleggini, M., Graziadei, L., Pedrinelli, R., Brandi, L., & Bevilacqua, S. (1987) · New England Journal of Medicine · doi:10.1056/nejm198708063170605 · Cited by 2,344
Kaplan, N. M. (1989) · Archives of Internal Medicine · doi:10.1001/archinte.149.7.1514 · Cited by 1,672
Metabolic Effects of Fructose and the Worldwide Increase in Obesity
Tappy, L., & Lê, K.-A. (2010) · Physiological Reviews · doi:10.1152/physrev.00019.2009 · Cited by 1,256
Prdm16 determines the thermogenic program of subcutaneous white adipose tissue in mice
Seale, P., Conroe, H. M., Estall, J. L., Kajimura, S., Frontini, A., Ishibashi, J., Cohen, P., Cinti, S., & Spiegelman, B. M. (2010) · Journal of Clinical Investigation · doi:10.1172/jci44271 · Cited by 1,273
Hyperinsulinemia produces both sympathetic neural activation and vasodilation in normal humans.
Anderson, E. A., Hoffman, R. P., Balon, T. W., Sinkey, C. A., & Mark, A. L. (1991) · Journal of Clinical Investigation · doi:10.1172/jci115260 · Cited by 1,075
Role of Insulin Resistance in Human Disease
Reaven, G. M. (1992) · Medical science symposia series · doi:10.1007/978-94-011-2700-4_10 · Cited by 895
Fructose-induced insulin resistance and hypertension in rats.
Hwang, I. S., Ho, H., Hoffman, B. B., & Reaven, G. M. (1987) · Hypertension · doi:10.1161/01.hyp.10.5.512 · Cited by 885
Cardiovascular Actions of Insulin
Muniyappa, R., Montagnani, M., Koh, K. K., & Quon, M. J. (2007) · Endocrine Reviews · doi:10.1210/er.2007-0006 · Cited by 888
“In healthy lean individuals, physiological concentrations of insulin increase venous catecholamine levels and sympathetic nerve activity (135, 156, 164).”
BackgroundHypothalamic insulin signaling is required for inhibition of glucose production
Obici, S., Zhang, B. B., Karkanias, G., & Rossetti, L. (2002) · Nature Medicine · doi:10.1038/nm1202-798 · Cited by 904
High-Fat, Western-Style Diet, Systemic Inflammation, and Gut Microbiota: A Narrative Review
Malesza, I. J., Malesza, M., Walkowiak, J., Mussin, N. M., Walkowiak, D., Aringazina, R. A., Bartkowiak-Wieczorek, J., & Mądry, E. (2021) · Cells · doi:10.3390/cells10113164 · Cited by 847
Diabetes and hypertension: the bad companions
Ferrannini, E., & Cushman, W. C. (2012) · The Lancet · doi:10.1016/s0140-6736(12)60987-8 · Cited by 705
How Western Diet And Lifestyle Drive The Pandemic Of Obesity And Civilization Diseases
Kopp, W. (2019) · Diabetes Metabolic Syndrome and Obesity · doi:10.2147/dmso.s216791 · Cited by 717
“There is a close relationship between insulin and the SNS: insulin activates the SNS in a dose-dependent manner in normal individuals, as indicated by elevated NE plasma levels (due to sympathetic nerve endings spillover) and micro-neurographic studies.(64) SNS activity is also influenced by food intake: among dietary…”
Esler, M., Jennings, G., Korner, P., Willett, I., Dudley, F., Hasking, G., Anderson, W., & Lambert, G. (1988) · Hypertension · doi:10.1161/01.hyp.11.1.3 · Cited by 642
Hemodynamic actions of insulin
Baron, A. (1994) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.1994.267.2.e187 · Cited by 611
Diabetes mellitus and hypertension.
Epstein, M., & Sowers, J. R. (1992) · Hypertension · doi:10.1161/01.hyp.19.5.403 · Cited by 626
Insulin and Atheroma: 20-Yr Perspective
Stout, R. W. (1990) · Diabetes Care · doi:10.2337/diacare.13.6.631 · Cited by 569
“These include an effect of insulin on renal sodium reabsorption (137) and enhanced sympathetic nervous system activity in hyperinsulinemic states (138,139), although this may not entirely explain raised blood pressure in obesity (140).”
Insulin resistance in chronic heart failure: relation to severity and etiology of heart failure.
Swan, J. W., Anker, S., Walton, C., Godsland, I., Clark, A., Leyva, F., Stevenson, J., & Coats, A. (1997) · Journal of the American College of Cardiology · doi:10.1016/s0735-1097(97)00185-x · Cited by 546
“In normal subjects infusion of insulin increases sympathetic activity (11), but infusions of either epinephrine or norepinephrine reduce insulin levels (12,13), suggesting a possible negative feedback mechanism.”
BackgroundInsulin resistance is a characteristic feature of primary hypertension independent of obesity
Pollare, T., Lithell, H., & Berne, C. (1990) · Metabolism · doi:10.1016/0026-0495(90)90071-j · Cited by 530
Landsberg, L., Aronne, L. J., Beilin, L. J., Burke, V., Igel, L. I., Lloyd‐Jones, D., & Sowers, J. (2013) · The Journal of Clinical Hypertension · doi:10.1111/jch.12049 · Cited by 528
Self-citationSympathetic Activation in the Pathogenesis of Hypertension and Progression of Organ Damage
Mancia, G., Grassi, G., Giannattasio, C., & Seravalle, G. (1999) · Hypertension · doi:10.1161/01.hyp.34.4.724 · Cited by 471
How to assess sympathetic activity in humans
Grassi, G., & Esler, M. (1999) · Journal of Hypertension · doi:10.1097/00004872-199917060-00001 · Cited by 455
Li, X., Dunn, J., Salins, D., Zhou, G., Zhou, W., Schüssler-Fiorenza Rose, S. M., Perelman, D., Colbert, E., Runge, R., Rego, S., et al. (2017) · PLOS Biology · doi:10.1371/journal.pbio.2001402 · Cited by 431
Adiposity, Fat Distribution, and Cardiovascular Risk
Peiris, A. N., Sothmann, M. S., Hoffmann, R. G., Hennes, M. I., Wilson, C. R., Gustafson, A. B., & Kissebah, A. H. (1989) · Annals of Internal Medicine · doi:10.7326/0003-4819-110-11-867 · Cited by 423
Racial Differences in the Relation between Blood Pressure and Insulin Resistance
Saad, M. F., Lillioja, S., Nyomba, B. L., Castillo, C., Ferraro, R., De Gregorio, M., Ravussin, E., Knowler, W. C., Bennett, P. H., Howard, B. V., et al. (1991) · New England Journal of Medicine · doi:10.1056/nejm199103143241105 · Cited by 421
Characterization of the insulin resistance of aging.
Rowe, J. W., Minaker, K. L., Pallotta, J. A., & Flier, J. S. (1983) · Journal of Clinical Investigation · doi:10.1172/jci110914 · Cited by 398
Self-citationBiology of regional body fat distribution: Relationship to non‐insulin‐dependent diabetes mellitus
Kissebah, A. H., & Peiris, A. N. (1989) · Diabetes/Metabolism Reviews · doi:10.1002/dmr.5610050202 · Cited by 384
LANDSBERG, L. (1986) · QJM: An International Journal of Medicine · doi:10.1093/oxfordjournals.qjmed.a068066 · Cited by 373
Self-citationScherrer, U., & Sartori, C. (1997) · Circulation · doi:10.1161/01.cir.96.11.4104 · Cited by 371
Grassi, G., Seravalle, G., Colombo, M., Bolla, G., Cattaneo, B. M., Cavagnini, F., & Mancia, G. (1998) · Circulation · doi:10.1161/01.cir.97.20.2037 · Cited by 364
Blood flow and muscle metabolism: a focus on insulin action
Clark, M. G., Wallis, M. G., Barrett, E. J., Keske, M. A., Richards, S. M., Clerk, L. H., & Rattigan, S. (2003) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.00408.2002 · Cited by 359
“There are several reports that insulin increases sympathetic nervous system (SNS) activity, as assessed by venous catecholamine levels (144) and forearm norepinephrine (NE) release (98) as well as by direct measurements of muscle sympathetic nerve activity (MSNA) (2, 190).”
BackgroundPollare, T., Lithell, H., Selinus, I., & Berne, C. (1988) · Diabetologia · doi:10.1007/bf00271585 · Cited by 354
Salt sensitivity in hypertension. Renal and cardiovascular implications.
Campese, V. M. (1994) · Hypertension · doi:10.1161/01.hyp.23.4.531 · Cited by 344
Grassi, G. M., Dell’Oro, R., Facchini, A., Trevano, F. Q., Bolla, G. B., & Mancia, G. (2004) · Journal of Hypertension · doi:10.1097/00004872-200412000-00019 · Cited by 339
Drazen, D. L., Vahl, T. P., D’Alessio, D. A., Seeley, R. J., & Woods, S. C. (2006) · Endocrinology · doi:10.1210/en.2005-0973 · Cited by 334
The Treatment of Hypertension in Adult Patients With Diabetes
Arauz-Pacheco, C., Parrott, M. A., & Raskin, P. (2002) · Diabetes Care · doi:10.2337/diacare.25.1.134 · Cited by 326
The eating paradox: How we tolerate food.
Woods, S. C. (1991) · Psychological Review · doi:10.1037/0033-295x.98.4.488 · Cited by 343
Vollenweider, P., Tappy, L., Randin, D., Schneiter, P., Jéquier, E., Nicod, P., & Scherrer, U. (1993) · Journal of Clinical Investigation · doi:10.1172/jci116542 · Cited by 321
Landsberg, L. (2001) · Journal of Hypertension · doi:10.1097/00004872-200103001-00001 · Cited by 312
Self-citationHyperinsulinaemia as a Risk Factor for Developing Benign Prostatic Hyperplasia
Hammarsten, J., & gstedt, B. H. O. (2001) · European Urology · doi:10.1159/000052430 · Cited by 305
Reflex sympathetic activation induces acute insulin resistance in the human forearm.
Jamerson, K. A., Julius, S., Gudbrandsson, T., Andersson, O., & Brant, D. O. (1993) · Hypertension · doi:10.1161/01.hyp.21.5.618 · Cited by 311
Insulin resistance and the metabolic syndrome
Landsberg, L. (2005) · Diabetologia · doi:10.1007/s00125-005-1818-z · Cited by 309
“It has been known for over two decades that insulin stimulates sympathetic activity [4] and, more recently, that this stimulation occurs at levels of insulin that are well within the physiological range [5].”
BackgroundSelf-citationLeggio, M., Lombardi, M., Caldarone, E., Severi, P., D’Emidio, S., Armeni, M., Bravi, V., Bendini, M. G., & Mazza, A. (2017) · Hypertension Research · doi:10.1038/hr.2017.75 · Cited by 319
Diabetes, Glucose, Insulin, and Heart Rate Variability
Schroeder, E. B., Chambless, L. E., Liao, D., Prineas, R. J., Evans, G. W., Rosamond, W. D., & Heiss, G. (2005) · Diabetes Care · doi:10.2337/diacare.28.3.668 · Cited by 302
Neuroadrenergic and reflex abnormalities in patients with metabolic syndrome
Grassi, G., Dell’Oro, R., Quarti-Trevano, F., Scopelliti, F., Seravalle, G., Paleari, F., Gamba, P. L., & Mancia, G. (2005) · Diabetologia · doi:10.1007/s00125-005-1798-z · Cited by 294
Reduced sympathetic nervous activity. A potential mechanism predisposing to body weight gain.
Spraul, M., Ravussin, E., Fontvieille, A. M., Rising, R., Larson, D. E., & Anderson, E. A. (1993) · Journal of Clinical Investigation · doi:10.1172/jci116760 · Cited by 293
Berne, C., Fagius, J., Pollare, T., & Hjemdahl, P. (1992) · Diabetologia · doi:10.1007/bf00399935 · Cited by 293
A ROLE FOR INSULIN IN THE AETIOLOGY AND COURSE OF HYPERTENSION?
Reaven, G. M., & Hoffman, B. B. (1987) · The Lancet · doi:10.1016/s0140-6736(87)90968-8 · Cited by 291
Role of the sympathetic nervous system in human hypertension
Grassi, G. M. (1998) · Journal of Hypertension · doi:10.1097/00004872-199816121-00019 · Cited by 286
Insulin stimulation of adipose tissue lipoprotein lipase. Use of the euglycemic clamp technique.
Sadur, C. N., & Eckel, R. H. (1982) · Journal of Clinical Investigation · doi:10.1172/jci110547 · Cited by 288
Insulin resistance and obesity in childhood
Chiarelli, F., & Marcovecchio, M. L. (2008) · European Journal of Endocrinology · doi:10.1530/eje-08-0245 · Cited by 294
Landsberg, L., Aronne, L. J., Beilin, L. J., Burke, V., Igel, L. I., Lloyd‐Jones, D. M., & Sowers, J. R. (2012) · Obesity · doi:10.1002/oby.20181 · Cited by 296
Self-citationOxidative stress and insulin action: is there a relationship?
Paolisso, G., & Giugliano, D. (1996) · Diabetologia · doi:10.1007/bf00418354 · Cited by 291
Insulin and renal sodium retention in obese adolescents.
Rocchini, A. P., Katch, V. L., Kveselis, D. A., Moorehead, C., Martin, M., Lampman, R. M., & Gregory, M. (1989) · Hypertension · doi:10.1161/01.hyp.14.4.367 · Cited by 274
“Other investigators have also shown that euglycemic hyperinsulinemia is associated with an acute increase in sympathetic tone.(27)-(29) Rowe et al(27) studied the effect of insulin and glucose infusions on sympathetic nervous system activity in 12 nonobese men.”
BackgroundEnhancement of insulin sensitivity by troglitazone lowers blood pressure in diabetic hypertensives
Ogihara, T., Rakugi, H., IKEGAMI, H., Mikami, H., & Masuo, K. (1995) · American Journal of Hypertension · doi:10.1016/0895-7061(95)96214-5 · Cited by 274
Postprandial Reduction in Blood Pressure in the Elderly
Lipsitz, L. A., Nyquist, R. P., Wei, J. Y., & Rowe, J. W. (1983) · New England Journal of Medicine · doi:10.1056/nejm198307143090205 · Cited by 274
Self-citationInsulin Infusion in Conscious Dogs
Liang, C., Doherty, J. U., FAILLACE, R. T., Maekawa, K., Arnold, S., Gavras, H. P., & Hood, W. B. (1982) · Journal of Clinical Investigation · doi:10.1172/jci110572 · Cited by 276
Insulin and blood pressure in obesity.
Lucas, C. P., Estigarribia, J., Darga, L. L., & Reaven, G. M. (1985) · Hypertension · doi:10.1161/01.hyp.7.5.702 · Cited by 273
“•* This viewpoint is bolstered by observations that short-term insulin administration to normal subjects results in sodium retention,(5)-(6) as well as increased blood pressure and heart rate.(7)”
BackgroundBrain glucose sensing and body energy homeostasis: role in obesity and diabetes
Levin, B. E., Dunn-Meynell, A. A., & Routh, V. H. (1999) · American Journal of Physiology-Regulatory, Integrative and Comparative Physiology · doi:10.1152/ajpregu.1999.276.5.r1223 · Cited by 272
“Relatively large intravenous or intracarotid glucose infusions produce generalized sympathetic nervous system activation in some humans (92) and animals (47, 48, 58–60) and this can be independent of changes in plasma insulin levels (47, 59).”
BackgroundRelation of obesity and diet to sympathetic nervous system activity.
Troisi, R. J., Weiss, S. T., Parker, D. R., Sparrow, D., Young, J. B., & Landsberg, L. (1991) · Hypertension · doi:10.1161/01.hyp.17.5.669 · Cited by 267
Self-citationGlucose intolerance, hyperinsulinaemia and cognitive function in a general population of elderly men
Kalmijn, S., Feskens, E. J. M., Launer, L. J., Stijnen, T., & Kromhout, D. (1995) · Diabetologia · doi:10.1007/bf00402181 · Cited by 274
“Hyperinsul inaemia might affect cognitive function through vascular processes regulated by the sympathetic nervous system [32] or by influencing synaptic activity in the brain [33].”
BackgroundSympathetic system activity in obesity and metabolic syndrome
TENTOLOURIS, N., LIATIS, S., & KATSILAMBROS, N. (2006) · Annals of the New York Academy of Sciences · doi:10.1196/annals.1367.010 · Cited by 260
Energy expenditure and postprandial thermogenesis in obese women before and after weight loss
Bessard, T., Schutz, Y., & Jéquier, E. (1983) · The American Journal of Clinical Nutrition · doi:10.1093/ajcn/38.5.680 · Cited by 257
Reaven, G. M. (1991) · American Heart Journal · doi:10.1016/0002-8703(91)90434-j · Cited by 253
Lembo, G., Napoli, R., Capaldo, B., Rendina, V, Iaccarino, G., Volpe, M., Trimarco, B., & Saccà, L. (1992) · Journal of Clinical Investigation · doi:10.1172/jci115842 · Cited by 252
Nutritional influences on lipogenesis and thermogenesis after a carbohydrate meal
Acheson, K. J., Schutz, Y., Bessard, T., Ravussin, É., Jéquier, E., & Flatt, J. P. (1984) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.1984.246.1.e62 · Cited by 254
Reducing Consumption of Sugar-Sweetened Beverages Is Associated With Reduced Blood Pressure
Chen, L., Caballero, B. H., Mitchell, D. C., Loria, C. M., Lin, P., Champagne, C. M., Elmer, P. J., Ard, J. D., Batch, B. C., Anderson, C. A. M., et al. (2010) · Circulation · doi:10.1161/circulationaha.109.911164 · Cited by 248
Lambert, É. (2011) · Frontiers in Physiology · doi:10.3389/fphys.2011.00052 · Cited by 243
“Furthermore, reflex and metabolic mechanisms may reinforce each other in the sympatho-inhibitory effect because insulin may lead to sympathetic activation through an impairment of the baroreceptor function (Rowe et al., 1981).”
BackgroundThe vasodilator action of insulin. Implications for the insulin hypothesis of hypertension.
Anderson, E. A., & Mark, A. L. (1993) · Hypertension · doi:10.1161/01.hyp.21.2.136 · Cited by 242
The Role of the Autonomic Nervous System in the Pathophysiology of Obesity
Guarino, D., Nannipieri, M., Iervasi, G., Taddei, S., & Bruno, R. M. (2017) · Frontiers in Physiology · doi:10.3389/fphys.2017.00665 · Cited by 259
“…has a direct vasodilatory effect during acute euglycemic hyperinsulinemic clamp: thus the increase in MSNA and norepinephrine levels reported in healthy individuals and hypertensive patients may be a consequence of baroreflex activation (Rowe et al., 1981; Anderson et al., 1991, 1992).”
BackgroundObesity and adipokines: effects on sympathetic overactivity
Smith, M. M., & Minson, C. T. (2012) · The Journal of Physiology · doi:10.1113/jphysiol.2011.221036 · Cited by 245
“Co-activation has been observed by measuring MSNA (Anderson et al. 1991; Berne et al. 1992; Vollenweider et al. 1995), plasma NA (Rowe et al. 1981; O’Hare et al. 1989; Berne et al. 1992; Vollenweider et al. 1995), or NA spillover (Lembo et al. 1992), during direct intracerebroventricular injection…”
MethodSympathoadrenal system and regulation of thermogenesis
Landsberg, L., Saville, M. E., & Young, J. B. (1984) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.1984.247.2.e181 · Cited by 232
Self-citationThermic effect of food and sympathetic nervous system activity in humans
Tappy, L. (1996) · annales de biologie animale biochimie biophysique · doi:10.1051/rnd:19960405 · Cited by 238
Abe, H., Yamada, N., Kamata, K., Kuwaki, T., Shimada, M., Osuga, J.-I., Shionoiri, F., Yahagi, N., Kadowaki, T., Tamemoto, H., et al. (1998) · Journal of Clinical Investigation · doi:10.1172/jci1594 · Cited by 229
“The mechanism associated with hypertension in insulin resistance with hyperinsulinemia may be related to skeletal muscle blood flow and relative skeletal muscle fiber type (22), vascular endothelial function (23), increased renal sodium reabsorption secondary to hyperinsulinemia (24), increased activity of the sympath…”
BackgroundFolsom, A. R., Prineas, R. J., Kaye, S. A., & Munger, R. G. (1990) · Stroke · doi:10.1161/01.str.21.5.701 · Cited by 229
Hyperinsulinemia and Autonomic Nervous System Dysfunction in Obesity
Emdin, M., Gastaldelli, A., Muscelli, E., Macerata, A., Natali, A., Camastra, S., & Ferrannini, E. (2001) · Circulation · doi:10.1161/01.cir.103.4.513 · Cited by 229
Insulin increases sympathetic activity but not blood pressure in borderline hypertensive humans.
Anderson, E. A., Balon, T. W., Hoffman, R. P., Sinkey, C. A., & Mark, A. L. (1992) · Hypertension · doi:10.1161/01.hyp.19.6.621 · Cited by 220
“Previous studies suggest that acute physiological increases in plasma insulin do not elevate arterial pressure in normotensive humans.(9)-(11) The current study demonstrates that acute physiological increases in plasma insulin produce marked sympathoexcitatory effects in borderline hypertensive humans but do not eleva…”
BackgroundInfluentialIs polycystic ovary syndrome associated with high sympathetic nerve activity and size at birth?
Sverrisdóttir, Y. B., Mogren, T., Kataoka, J., Janson, P. O., & Stener-Victorin, E. (2008) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.00725.2007 · Cited by 216
“Peripheral cardiovascular risk factors such as abdominal obesity, dyslipedemia, glucose intolerance, and insulin resistance (34), known to be associated with PCOS, may per se provoke changes in sympathetic nerve activity (8, 20, 21, 35, 41).”
BackgroundRisk factors for developing non-insulin dependent diabetes: a 10 year follow up of men in Uppsala.
Skarfors, E., Selinus, K. I., & Lithell, H. (1991) · BMJ · doi:10.1136/bmj.303.6805.755 · Cited by 212
The role of insulin in clustering of serum lipids and blood pressure in children and adolescents
Raitakari, O. T., Porkka, K., R�nnemaa, T., Knip, M., Uhari, M. K., �kerblom, H. K., & Viikari, J. S. A. (1995) · Diabetologia · doi:10.1007/bf00402173 · Cited by 215
Thermic effect of glucose in man. Obligatory and facultative thermogenesis.
Acheson, K. J., Ravussin, E., Wahren, J., & Jéquier, E. (1984) · Journal of Clinical Investigation · doi:10.1172/jci111573 · Cited by 209
Ferrari, P., Weidmann, P. U., Shaw, S., Giachino, D., Riesen, W., Allemann, Y., & Heynen, G. (1991) · The American Journal of Medicine · doi:10.1016/0002-9343(91)90211-f · Cited by 207
Brief Review: Hypertension in Pregnancy
Solomon, C. G., & Seely, E. W. (2001) · Hypertension · doi:10.1161/01.hyp.37.2.232 · Cited by 207
Sugar-Sweetened Beverage, Sugar Intake of Individuals, and Their Blood Pressure
Brown, I., Stamler, J., Horn, L. V., Robertson, C. E., Chan, Q. M., Dyer, A. R., Huang, C., Rodríguez, B. L., Zhao, L., Daviglus, M. L., et al. (2011) · Hypertension · doi:10.1161/hypertensionaha.110.165456 · Cited by 206
Louis K. Dahl Memorial Lecture. Renal and cardiovascular mechanisms of hypertension in obesity.
Hall, J. E. (1994) · Hypertension · doi:10.1161/01.hyp.23.3.381 · Cited by 204
Clustering of cardiovascular risk factors in confirmed prehypertensive individuals.
Haffner, S. M., Ferrannini, E., Hazuda, H. P., & Stern, M. P. (1992) · Hypertension · doi:10.1161/01.hyp.20.1.38 · Cited by 195
Are Metabolic Risk Factors One Unified Syndrome? Modeling the Structure of the Metabolic Syndrome X
Shen, B. (2003) · American Journal of Epidemiology · doi:10.1093/aje/kwg045 · Cited by 203
Zemel, M. B. (1998) · Springer eBooks · doi:10.1007/978-1-4615-5763-0_14 · Cited by 194
Insulin resistance, insulin response, and obesity as indicators of metabolic risk
Ferrannini, E., Balkau, B., Coppack, S. W., Dekker, J. M., Mari, A., Nolan, J., Walker, M., Natali, A., & Beck-Nielsen, H. (2007) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2007-0334 · Cited by 193
“The association of a higher resting heart rate with hyperinsulinemia may reflect the ability of insulin to stimulate the sympathetic nervous system (36).”
BackgroundBianchi, S., Bigazzi, R., & Campese, V. M. (1999) · American Journal of Kidney Diseases · doi:10.1016/s0272-6386(99)70002-8 · Cited by 185
Hypothalamic PI3K and MAPK differentially mediate regional sympathetic activation to insulin
Rahmouni, K., Morgan, D. A., Morgan, G. M., Liu, X., Sigmund, C. D., Mark, A. L., & Haynes, W. G. (2004) · Journal of Clinical Investigation · doi:10.1172/jci21737 · Cited by 187
Berne, C., Fagius, J., & Niklasson, F. (1989) · Journal of Clinical Investigation · doi:10.1172/jci114313 · Cited by 182
HAMMARSTEN, B. H. J. (1999) · Blood Pressure · doi:10.1080/080370599438365 · Cited by 182
Metabolic Syndrome and CKD in a General Japanese Population: The Hisayama Study
Ninomiya, T., Kiyohara, Y., Kubo, M., Yonemoto, K., Tanizaki, Y., Doi, Y., Hirakata, H., & Iida, M. (2006) · American Journal of Kidney Diseases · doi:10.1053/j.ajkd.2006.06.003 · Cited by 181
Insulin differentially regulates systemic and skeletal muscle vascular resistance
Baron, A., & Brechtel, G. (1993) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.1993.265.1.e61 · Cited by 179
Ravussin, E., Bogardus, C., Schwartz, R. S., Robbins, D. C., Wolfe, R. R., Horton, E. S., Danforth, E., & Sims, E. A. (1983) · Journal of Clinical Investigation · doi:10.1172/jci111060 · Cited by 172
Influence of beta-adrenergic blockade on glucose-induced thermogenesis in man.
Acheson, K., Jéquier, E., & Wahren, J. (1983) · Journal of Clinical Investigation · doi:10.1172/jci111070 · Cited by 171
Insulin Resistance in Patients with Chronic Kidney Disease
Liao, M.-T., Sung, C., Hung, K.-C., Wu, C., Lo, L., & Lu, K. (2012) · BioMed Research International · doi:10.1155/2012/691369 · Cited by 180
“IR promotes kidney disease by worsening renal hemodynamics through mechanisms such as activation of the sympathetic nervous system [26], sodium retention, decreased Na+, K+-ATPase activity, and increased GFR [24].”
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 ›
Are you an author, or do you see a problem with this page? Request a review