Human Type 1 Diabetes Is Characterized by an Early, Marked, Sustained, and Islet-Selective Loss of Sympathetic Nerves

In humans, the glucagon response to moderate-to-marked insulin-induced hypoglycemia (IIH) is largely mediated by the autonomic nervous system. Because this glucagon response is impaired early in type 1 diabetes, we sought to determine if these patients, like animal models of autoimmune diabetes, hav...

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Published inDiabetes (New York, N.Y.) Vol. 65; no. 8; pp. 2322 - 2330
Main Authors Mundinger, Thomas O., Mei, Qi, Foulis, Alan K., Fligner, Corinne L., Hull, Rebecca L., Taborsky, Gerald J.
Format Journal Article
LanguageEnglish
Published United States American Diabetes Association 01.08.2016
Subjects
Adolescent
Adult
Autonomic Nervous System - metabolism
Autonomic Nervous System - pathology
Autonomic Nervous System - physiopathology
Child
Diabetes
Diabetes Mellitus, Type 1 - metabolism
Diabetes Mellitus, Type 1 - pathology
Diabetes Mellitus, Type 1 - physiopathology
Diabetes Mellitus, Type 2 - metabolism
Diabetes Mellitus, Type 2 - pathology
Diabetes Mellitus, Type 2 - physiopathology
Female
Glucagon - metabolism
Humans
Hypoglycemia
Hypoglycemia - metabolism
Hypoglycemia - pathology
Hypoglycemia - physiopathology
Immunohistochemistry
Insulin
Islet Studies
Islets of Langerhans - metabolism
Islets of Langerhans - pathology
Islets of Langerhans - physiopathology
Male
Middle Aged
Nervous system
Pancreas - metabolism
Pancreas - pathology
Pancreas - physiopathology
Sympathetic Nervous System - metabolism
Sympathetic Nervous System - pathology
Sympathetic Nervous System - physiopathology
Young Adult
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Abstract In humans, the glucagon response to moderate-to-marked insulin-induced hypoglycemia (IIH) is largely mediated by the autonomic nervous system. Because this glucagon response is impaired early in type 1 diabetes, we sought to determine if these patients, like animal models of autoimmune diabetes, have an early and severe loss of islet sympathetic nerves. We also tested whether this nerve loss is a permanent feature of type 1 diabetes, is islet-selective, and is not seen in type 2 diabetes. To do so, we quantified pancreatic islet and exocrine sympathetic nerve fiber area from autopsy samples of patients with type 1 or 2 diabetes and control subjects without diabetes. Our central finding is that patients with either very recent onset (<2 weeks) or long duration (>10 years) of type 1 diabetes have a severe loss of islet sympathetic nerves (Δ = −88% and Δ = −79%, respectively). In contrast, patients with type 2 diabetes lose no islet sympathetic nerves. There is no loss of exocrine sympathetic nerves in either type 1 or type 2 diabetes. We conclude that patients with type 1, but not type 2, diabetes have an early, marked, sustained, and islet-selective loss of sympathetic nerves, one that may impair their glucagon response to IIH.
AbstractList In humans, the glucagon response to moderate-to-marked insulin-induced hypoglycemia (IIH) is largely mediated by the autonomic nervous system. Because this glucagon response is impaired early in type 1 diabetes, we sought to determine if these patients, like animal models of autoimmune diabetes, have an early and severe loss of islet sympathetic nerves. We also tested whether this nerve loss is a permanent feature of type 1 diabetes, is islet-selective, and is not seen in type 2 diabetes. To do so, we quantified pancreatic islet and exocrine sympathetic nerve fiber area from autopsy samples of patients with type 1 or 2 diabetes and control subjects without diabetes. Our central finding is that patients with either very recent onset (<2 weeks) or long duration (>10 years) of type 1 diabetes have a severe loss of islet sympathetic nerves (Δ = -88% and Δ = -79%, respectively). In contrast, patients with type 2 diabetes lose no islet sympathetic nerves. There is no loss of exocrine sympathetic nerves in either type 1 or type 2 diabetes. We conclude that patients with type 1, but not type 2, diabetes have an early, marked, sustained, and islet-selective loss of sympathetic nerves, one that may impair their glucagon response to IIH.
In humans, the glucagon response to moderate-to-marked insulin-induced hypoglycemia (IIH) is largely mediated by the autonomic nervous system. Because this glucagon response is impaired early in type 1 diabetes, we sought to determine if these patients, like animal models of autoimmune diabetes, have an early and severe loss of islet sympathetic nerves. We also tested whether this nerve loss is a permanent feature of type 1 diabetes, is islet-selective, and is not seen in type 2 diabetes. To do so, we quantified pancreatic islet and exocrine sympathetic nerve fiber area from autopsy samples of patients with type 1 or 2 diabetes and control subjects without diabetes. Our central finding is that patients with either very recent onset (<2 weeks) or long duration (>10 years) of type 1 diabetes have a severe loss of islet sympathetic nerves (Δ = −88% and Δ = −79%, respectively). In contrast, patients with type 2 diabetes lose no islet sympathetic nerves. There is no loss of exocrine sympathetic nerves in either type 1 or type 2 diabetes. We conclude that patients with type 1, but not type 2, diabetes have an early, marked, sustained, and islet-selective loss of sympathetic nerves, one that may impair their glucagon response to IIH.
In humans, the glucagon response to moderate-to-marked insulin-induced hypoglycemia (IIH) is largely mediated by the autonomic nervous system. Because this glucagon response is impaired early in type 1 diabetes, we sought to determine if these patients, like animal models of autoimmune diabetes, have an early and severe loss of islet sympathetic nerves. We also tested whether this nerve loss is a permanent feature of type 1 diabetes, is islet-selective, and is not seen in type 2 diabetes. To do so, we quantified pancreatic islet and exocrine sympathetic nerve fiber area from autopsy samples of patients with type 1 or 2 diabetes and control subjects without diabetes. Our central finding is that patients with either very recent onset (<2 weeks) or long duration (>10 years) of type 1 diabetes have a severe loss of islet sympathetic nerves (Δ = -88% and Δ = -79%, respectively). In contrast, patients with type 2 diabetes lose no islet sympathetic nerves. There is no loss of exocrine sympathetic nerves in either type 1 or type 2 diabetes. We conclude that patients with type 1, but not type 2, diabetes have an early, marked, sustained, and islet-selective loss of sympathetic nerves, one that may impair their glucagon response to IIH.In humans, the glucagon response to moderate-to-marked insulin-induced hypoglycemia (IIH) is largely mediated by the autonomic nervous system. Because this glucagon response is impaired early in type 1 diabetes, we sought to determine if these patients, like animal models of autoimmune diabetes, have an early and severe loss of islet sympathetic nerves. We also tested whether this nerve loss is a permanent feature of type 1 diabetes, is islet-selective, and is not seen in type 2 diabetes. To do so, we quantified pancreatic islet and exocrine sympathetic nerve fiber area from autopsy samples of patients with type 1 or 2 diabetes and control subjects without diabetes. Our central finding is that patients with either very recent onset (<2 weeks) or long duration (>10 years) of type 1 diabetes have a severe loss of islet sympathetic nerves (Δ = -88% and Δ = -79%, respectively). In contrast, patients with type 2 diabetes lose no islet sympathetic nerves. There is no loss of exocrine sympathetic nerves in either type 1 or type 2 diabetes. We conclude that patients with type 1, but not type 2, diabetes have an early, marked, sustained, and islet-selective loss of sympathetic nerves, one that may impair their glucagon response to IIH.
In humans, the glucagon response to moderate-to-marked insulin-induced hypoglycemia (IIH) is largely mediated by the autonomic nervous system. Because this glucagon response is impaired early in type 1 diabetes, we sought to determine if these patients, like animal models of autoimmune diabetes, have an early and severe loss of islet sympathetic nerves. We also tested whether this nerve loss is a permanent feature of type 1 diabetes, is islet-selective, and is not seen in type 2 diabetes. To do so, we quantified pancreatic islet and exocrine sympathetic nerve fiber area from autopsy samples of patients with type 1 or 2 diabetes and control subjects without diabetes. Our central finding is that patients with either very recent onset (<2 weeks) or long duration (>10 years) of type 1 diabetes have a severe loss of islet sympathetic nerves ( Delta = -88% and Delta = -79%, respectively). In contrast, patients with type 2 diabetes lose no islet sympathetic nerves. There is no loss of exocrine sympathetic nerves in either type 1 or type 2 diabetes. We conclude that patients with type 1, but not type 2, diabetes have an early, marked, sustained, and islet-selective loss of sympathetic nerves, one that may impair their glucagon response to IIH.
In humans, the glucagon response to moderate-to-marked insulin-induced hypoglycemia (IIH) is largely mediated by the autonomic nervous system. Because this glucagon response is impaired early in type 1 diabetes, we sought to determine if these patients, like animal models of autoimmune diabetes, have an early and severe loss of islet sympathetic nerves. We also tested whether this nerve loss is a permanent feature of type 1 diabetes, is islet-selective, and is not seen in type 2 diabetes. To do so, we quantified pancreatic islet and exocrine sympathetic nerve fiber area from autopsy samples of patients with type 1 or 2 diabetes and control subjects without diabetes. Our central finding is that patients with either very recent onset (<2 weeks) or long duration (>10 years) of type 1 diabetes have a severe loss of islet sympathetic nerves (... = -88% and ... = -79%, respectively). In contrast, patients with type 2 diabetes lose no islet sympathetic nerves. There is no loss of exocrine sympathetic nerves in either type 1 or type 2 diabetes. We conclude that patients with type 1, but not type 2, diabetes have an early, marked, sustained, and islet-selective loss of sympathetic nerves, one that may impair their glucagon response to IIH. (ProQuest: ... denotes formulae/symbols omitted.)
Author Mundinger, Thomas O.
Mei, Qi
Hull, Rebecca L.
Fligner, Corinne L.
Taborsky, Gerald J.
Foulis, Alan K.
Author_xml – sequence: 1
  givenname: Thomas O.
  surname: Mundinger
  fullname: Mundinger, Thomas O.
  organization: Department of Medicine, University of Washington, Seattle, WA
– sequence: 2
  givenname: Qi
  surname: Mei
  fullname: Mei, Qi
  organization: Department of Medicine, University of Washington, Seattle, WA
– sequence: 3
  givenname: Alan K.
  surname: Foulis
  fullname: Foulis, Alan K.
  organization: Department of Pathology, Southern General Hospital, Glasgow, Scotland, U.K
– sequence: 4
  givenname: Corinne L.
  surname: Fligner
  fullname: Fligner, Corinne L.
  organization: Department of Pathology, University of Washington, Seattle, WA
– sequence: 5
  givenname: Rebecca L.
  surname: Hull
  fullname: Hull, Rebecca L.
  organization: Department of Medicine, University of Washington, Seattle, WA, VA Puget Sound Health Care System, Seattle, WA
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  givenname: Gerald J.
  surname: Taborsky
  fullname: Taborsky, Gerald J.
  organization: Department of Medicine, University of Washington, Seattle, WA, VA Puget Sound Health Care System, Seattle, WA
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Cites_doi 10.1152/ajpendo.00136.2003
10.1002/(SICI)1097-4598(199810)21:10<1246::AID-MUS2>3.0.CO;2-B
10.1530/acta.0.0980402
10.2337/diab.32.2.134
10.1172/JCI108992
10.1113/jphysiol.1981.sp013730
10.2337/diacare.6.1.95
10.1172/JCI108460
10.1089/152091501750219985
10.1111/j.1748-1716.1981.tb06698.x
10.1210/jc.2007-0536
10.2337/dc10-1303
10.2337/diacare.28.4.956
10.2337/diab.37.4.476
10.1016/j.cmet.2011.06.004
10.1016/j.diabet.2012.10.006
10.1210/jcem-37-3-479
10.1007/BF01239960
10.1210/endo-121-1-323
10.1111/j.1085-9489.2005.0010205.x
10.1210/jcem-44-3-459
10.2337/diab.34.9.870
10.2337/db15-0779
10.1038/nrneurol.2013.227
10.1056/NEJMoa1111732
10.1007/BF00870137
10.1113/jphysiol.1978.sp012370
10.1038/414813a
10.2337/diabetes.51.10.2997
10.1056/NEJMoa052187
10.1210/edrv-10-3-332
10.1210/en.2011-2040
10.1007/BF00295875
10.1126/science.182.4108.171
10.1016/j.cmet.2011.05.008
10.1172/JCI107292
10.2337/db13-0778
10.1056/NEJM199309303291401
10.1172/JCI113763
10.1007/s00125-009-1494-5
10.2337/diabetes.47.7.995
10.1038/nri2192
10.1038/nrendo.2013.131
10.2337/diabetes.50.2.217
10.1111/j.1365-2249.2008.03860.x
10.1038/nn.2114
10.1056/NEJMoa1409463
10.2337/diab.44.12.1355
10.2337/diab.46.5.801
10.1016/0735-1097(94)00459-4
10.1016/S0140-6736(98)07019-6
10.1111/pedi.12070
ContentType Journal Article
Copyright 2016 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered.
Copyright American Diabetes Association Aug 1, 2016
2016 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. 2016
Copyright_xml – notice: 2016 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered.
– notice: Copyright American Diabetes Association Aug 1, 2016
– notice: 2016 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. 2016
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References Havel (2022031300065618700_B12) 1996; 270
Langer (2022031300065618700_B30) 1995; 25
Nathan (2022031300065618700_B9) 2005; 353
Heller (2022031300065618700_B53) 1987; 30
UK Prospective Diabetes Study (UKPDS) Group (2022031300065618700_B33) 1998; 352
Ahrén (2022031300065618700_B18) 1986; 29
Böhme (2022031300065618700_B5) 2013; 39
Taborsky (2022031300065618700_B25) 2009; 52
Stevens (2022031300065618700_B29) 2001; 3
Velloso (2022031300065618700_B37) 2013; 9
Rodriguez-Diaz (2022031300065618700_B44) 2011; 14
Bloom (2022031300065618700_B50) 1978; 280
Taborsky (2022031300065618700_B46) 2011; 14
Havel (2022031300065618700_B48) 1988; 82
Gerich (2022031300065618700_B1) 1973; 182
Campbell-Thompson (2022031300065618700_B38) 2016; 65
Boulton (2022031300065618700_B28) 2005; 28
Quasthoff (2022031300065618700_B56) 1998; 21
Schwartz (2022031300065618700_B11) 1978; 61
Bolli (2022031300065618700_B23) 1983; 32
Garber (2022031300065618700_B13) 1976; 58
Gilliam (2022031300065618700_B45) 2007; 92
Pettersson (2022031300065618700_B43) 1987; 248
Holst (2022031300065618700_B51) 1981; 111
Taborsky (2022031300065618700_B20) 2012; 153
Arbelaez (2022031300065618700_B3) 2014; 15
Marliss (2022031300065618700_B15) 1973; 52
Cryer (2022031300065618700_B4) 1983; 6
Kennedy (2022031300065618700_B42) 2005; 10
Bloom (2022031300065618700_B16) 1981; 315
Taborsky (2022031300065618700_B26) 2014; 63
Tesfaye (2022031300065618700_B27) 2010; 33
Scheib (2022031300065618700_B41) 2013; 9
Schmidt (2022031300065618700_B31) 1983; 49
Brownlee (2022031300065618700_B34) 2001; 414
Havel (2022031300065618700_B14) 1989; 10
Aiello (2022031300065618700_B7) 2015; 372
Pfeifer (2022031300065618700_B55) 1995; 44
Havel (2022031300065618700_B10) 1997; 46
Järhult (2022031300065618700_B21) 1981; 98
The Diabetes Control and Complications Trial Research Group (2022031300065618700_B6) 1993; 329
Taborsky (2022031300065618700_B19) 1998; 47
Gale (2022031300065618700_B36) 2001; 50
Dunning (2022031300065618700_B49) 1997; 272
Ahrén (2022031300065618700_B52) 1987; 121
Willcox (2022031300065618700_B40) 2009; 155
Gerich (2022031300065618700_B17) 1973; 37
Benson (2022031300065618700_B2) 1977; 44
de Boer (2022031300065618700_B8) 2011; 365
von Herrath (2022031300065618700_B39) 2007; 7
2022031300065618700_B54
Mundinger (2022031300065618700_B47) 2003; 285
White (2022031300065618700_B22) 1985; 34
Singh (2022031300065618700_B35) 2008; 11
Mei (2022031300065618700_B24) 2002; 51
The DCCT Research Group (2022031300065618700_B32) 1988; 37
15958126 - J Peripher Nerv Syst. 2005 Jun;10(2):144-57
7589838 - Diabetes. 1995 Dec;44(12):1355-61
16371630 - N Engl J Med. 2005 Dec 22;353(25):2643-53
25410245 - Handb Clin Neurol. 2014;126:579-602
9176171 - Am J Physiol. 1997 May;272(5 Pt 1):E746-55
12351439 - Diabetes. 2002 Oct;51(10):2997-3002
25923552 - N Engl J Med. 2015 Apr 30;372(18):1722-33
23992543 - Pediatr Diabetes. 2014 Mar;15(2):127-34
3183052 - J Clin Invest. 1988 Nov;82(5):1538-45
6337896 - Diabetes. 1983 Feb;32(2):134-41
22077236 - N Engl J Med. 2011 Dec 22;365(25):2366-76
2993084 - Diabetes. 1985 Sep;34(9):870-5
7860904 - J Am Coll Cardiol. 1995 Mar 1;25(3):610-8
6341018 - Diabetes Care. 1983 Jan-Feb;6(1):95-9
11469712 - Diabetes Technol Ther. 2001 Spring;3(1):9-22
838846 - J Clin Endocrinol Metab. 1977 Mar;44(3):459-64
24608438 - Diabetes. 2014 Jul;63(7):2369-79
6632773 - Lab Invest. 1983 Nov;49(5):538-52
2897940 - Diabetes. 1988 Apr;37(4):476-81
9736052 - Muscle Nerve. 1998 Oct;21(10):1246-55
3297643 - Endocrinology. 1987 Jul;121(1):323-31
11742414 - Nature. 2001 Dec 13;414(6865):813-20
21723498 - Cell Metab. 2011 Jul 6;14(1):5-6
26581594 - Diabetes. 2016 Mar;65(3):719-31
23266467 - Diabetes Metab. 2013 Feb;39(1):63-70
18382462 - Nat Neurosci. 2008 Jun;11(6):649-58
6491 - J Clin Invest. 1976 Jul;58(1):7-15
3325324 - Diabetologia. 1987 Dec;30(12):924-9
7027713 - Acta Endocrinol (Copenh). 1981 Nov;98(3):402-6
3552240 - Cell Tissue Res. 1987 Apr;248(1):43-8
19128359 - Clin Exp Immunol. 2009 Feb;155(2):173-81
12876072 - Am J Physiol Endocrinol Metab. 2003 Nov;285(5):E1047-54
24217518 - Nat Rev Neurol. 2013 Dec;9(12):668-76
9742976 - Lancet. 1998 Sep 12;352(9131):837-53
23835371 - Nat Rev Endocrinol. 2013 Dec;9(12):750-5
15793206 - Diabetes Care. 2005 Apr;28(4):956-62
4349486 - J Clin Invest. 1973 May;52(5):1246-59
21723503 - Cell Metab. 2011 Jul 6;14(1):45-54
7031230 - J Physiol. 1981 Jun;315:31-41
9648820 - Diabetes. 1998 Jul;47(7):995-1005
8366922 - N Engl J Med. 1993 Sep 30;329(14):977-86
8772469 - Am J Physiol. 1996 Jan;270(1 Pt 1):E20-6
9133547 - Diabetes. 1997 May;46(5):801-7
11272129 - Diabetes. 2001 Feb;50(2):217-26
690873 - J Physiol. 1978 Jul;280:25-35
641155 - J Clin Invest. 1978 Mar;61(3):781-9
19798480 - Diabetologia. 2009 Dec;52(12):2602-11
4581053 - Science. 1973 Oct 12;182(4108):171-3
22315452 - Endocrinology. 2012 Mar;153(3):1055-62
2883061 - Diabetologia. 1986 Dec;29(12):827-36
6111894 - Acta Physiol Scand. 1981 Jan;111(1):9-14
20876709 - Diabetes Care. 2010 Oct;33(10):2285-93
17684049 - J Clin Endocrinol Metab. 2007 Oct;92(10):4035-8
4785433 - J Clin Endocrinol Metab. 1973 Sep;37(3):479-81
17982429 - Nat Rev Immunol. 2007 Dec;7(12):988-94
2673755 - Endocr Rev. 1989 Aug;10(3):332-50
References_xml – volume: 285
  start-page: E1047
  year: 2003
  ident: 2022031300065618700_B47
  article-title: Impaired glucagon response to sympathetic nerve stimulation in the BB diabetic rat: effect of early sympathetic islet neuropathy
  publication-title: Am J Physiol Endocrinol Metab
  doi: 10.1152/ajpendo.00136.2003
– volume: 21
  start-page: 1246
  year: 1998
  ident: 2022031300065618700_B56
  article-title: The role of axonal ion conductances in diabetic neuropathy: a review
  publication-title: Muscle Nerve
  doi: 10.1002/(SICI)1097-4598(199810)21:10<1246::AID-MUS2>3.0.CO;2-B
– volume: 270
  start-page: E20
  year: 1996
  ident: 2022031300065618700_B12
  article-title: Pancreatic sympathetic nerves contribute to increased glucagon secretion during severe hypoglycemia in dogs
  publication-title: Am J Physiol
– volume: 98
  start-page: 402
  year: 1981
  ident: 2022031300065618700_B21
  article-title: The relation between catecholamines, glucagon and pancreatic polypeptide during hypoglycaemia in man
  publication-title: Acta Endocrinol (Copenh)
  doi: 10.1530/acta.0.0980402
– volume: 272
  start-page: E746
  year: 1997
  ident: 2022031300065618700_B49
  article-title: Direct quantification of norepinephrine spillover and hormone output from the pancreas of the conscious dog
  publication-title: Am J Physiol
– volume: 32
  start-page: 134
  year: 1983
  ident: 2022031300065618700_B23
  article-title: Abnormal glucose counterregulation in insulin-dependent diabetes mellitus. Interaction of anti-insulin antibodies and impaired glucagon and epinephrine secretion
  publication-title: Diabetes
  doi: 10.2337/diab.32.2.134
– volume: 61
  start-page: 781
  year: 1978
  ident: 2022031300065618700_B11
  article-title: Vagal, cholinergic regulation of pancreatic polypeptide secretion
  publication-title: J Clin Invest
  doi: 10.1172/JCI108992
– volume: 315
  start-page: 31
  year: 1981
  ident: 2022031300065618700_B16
  article-title: Pancreatic endocrine responses to stimulation of the peripheral ends of the vagus nerves in conscious calves
  publication-title: J Physiol
  doi: 10.1113/jphysiol.1981.sp013730
– volume: 6
  start-page: 95
  year: 1983
  ident: 2022031300065618700_B4
  article-title: Relevance of glucose counterregulatory systems to patients with diabetes: critical roles of glucagon and epinephrine
  publication-title: Diabetes Care
  doi: 10.2337/diacare.6.1.95
– volume: 58
  start-page: 7
  year: 1976
  ident: 2022031300065618700_B13
  article-title: The role of adrenergic mechanisms in the substrate and hormonal response to insulin-induced hypoglycemia in man
  publication-title: J Clin Invest
  doi: 10.1172/JCI108460
– volume: 3
  start-page: 9
  year: 2001
  ident: 2022031300065618700_B29
  article-title: New imaging techniques for cardiovascular autonomic neuropathy: a window on the heart
  publication-title: Diabetes Technol Ther
  doi: 10.1089/152091501750219985
– volume: 111
  start-page: 9
  year: 1981
  ident: 2022031300065618700_B51
  article-title: Nervous control of pancreatic endocrine secretion in pigs. II. The effect of pharmacological blocking agents on the response to vagal stimulation
  publication-title: Acta Physiol Scand
  doi: 10.1111/j.1748-1716.1981.tb06698.x
– volume: 92
  start-page: 4035
  year: 2007
  ident: 2022031300065618700_B45
  article-title: Tyramine-mediated activation of sympathetic nerves inhibits insulin secretion in humans
  publication-title: J Clin Endocrinol Metab
  doi: 10.1210/jc.2007-0536
– volume: 33
  start-page: 2285
  year: 2010
  ident: 2022031300065618700_B27
  article-title: Diabetic neuropathies: update on definitions, diagnostic criteria, estimation of severity, and treatments
  publication-title: Diabetes Care
  doi: 10.2337/dc10-1303
– volume: 49
  start-page: 538
  year: 1983
  ident: 2022031300065618700_B31
  article-title: Experimental diabetic autonomic neuropathy characterization in streptozotocin-diabetic Sprague-Dawley rats
  publication-title: Lab Invest
– volume: 28
  start-page: 956
  year: 2005
  ident: 2022031300065618700_B28
  article-title: Diabetic neuropathies: a statement by the American Diabetes Association
  publication-title: Diabetes Care
  doi: 10.2337/diacare.28.4.956
– volume: 37
  start-page: 476
  year: 1988
  ident: 2022031300065618700_B32
  article-title: Factors in development of diabetic neuropathy. Baseline analysis of neuropathy in feasibility phase of Diabetes Control and Complications Trial (DCCT)
  publication-title: Diabetes
  doi: 10.2337/diab.37.4.476
– volume: 14
  start-page: 5
  year: 2011
  ident: 2022031300065618700_B46
  article-title: Islets have a lot of nerve! Or do they?
  publication-title: Cell Metab
  doi: 10.1016/j.cmet.2011.06.004
– volume: 39
  start-page: 63
  year: 2013
  ident: 2022031300065618700_B5
  article-title: Fear of hypoglycaemia in patients with type 1 diabetes: do patients and diabetologists feel the same way?
  publication-title: Diabetes Metab
  doi: 10.1016/j.diabet.2012.10.006
– volume: 37
  start-page: 479
  year: 1973
  ident: 2022031300065618700_B17
  article-title: Stimulation of glucagon secretion by epinephrine in man
  publication-title: J Clin Endocrinol Metab
  doi: 10.1210/jcem-37-3-479
– volume: 248
  start-page: 43
  year: 1987
  ident: 2022031300065618700_B43
  article-title: Neuropeptide Y: intrapancreatic neuronal localization and effects on insulin secretion in the mouse
  publication-title: Cell Tissue Res
  doi: 10.1007/BF01239960
– volume: 121
  start-page: 323
  year: 1987
  ident: 2022031300065618700_B52
  article-title: Sympathetic nerve stimulation versus pancreatic norepinephrine infusion in the dog: 1). Effects on basal release of insulin and glucagon
  publication-title: Endocrinology
  doi: 10.1210/endo-121-1-323
– volume: 10
  start-page: 144
  year: 2005
  ident: 2022031300065618700_B42
  article-title: Impaired peripheral nerve regeneration in diabetes mellitus
  publication-title: J Peripher Nerv Syst
  doi: 10.1111/j.1085-9489.2005.0010205.x
– volume: 44
  start-page: 459
  year: 1977
  ident: 2022031300065618700_B2
  article-title: Glucagon and catecholamine secretion during hypoglycemia in normal and diabetic man
  publication-title: J Clin Endocrinol Metab
  doi: 10.1210/jcem-44-3-459
– volume: 34
  start-page: 870
  year: 1985
  ident: 2022031300065618700_B22
  article-title: Plasma pancreatic polypeptide response to insulin-induced hypoglycemia as a marker for defective glucose counterregulation in insulin-dependent diabetes mellitus
  publication-title: Diabetes
  doi: 10.2337/diab.34.9.870
– volume: 65
  start-page: 719
  year: 2016
  ident: 2022031300065618700_B38
  article-title: Insulitis and β-cell mass in the natural history of type 1 diabetes
  publication-title: Diabetes
  doi: 10.2337/db15-0779
– volume: 9
  start-page: 668
  year: 2013
  ident: 2022031300065618700_B41
  article-title: Advances in peripheral nerve regeneration
  publication-title: Nat Rev Neurol
  doi: 10.1038/nrneurol.2013.227
– volume: 365
  start-page: 2366
  year: 2011
  ident: 2022031300065618700_B8
  article-title: Intensive diabetes therapy and glomerular filtration rate in type 1 diabetes
  publication-title: N Engl J Med
  doi: 10.1056/NEJMoa1111732
– volume: 29
  start-page: 827
  year: 1986
  ident: 2022031300065618700_B18
  article-title: Neuropeptidergic versus cholinergic and adrenergic regulation of islet hormone secretion
  publication-title: Diabetologia
  doi: 10.1007/BF00870137
– volume: 280
  start-page: 25
  year: 1978
  ident: 2022031300065618700_B50
  article-title: Certain pharmacological characteristics of the release of pancreatic glucagon in response to stimulation of the splanchnic nerves
  publication-title: J Physiol
  doi: 10.1113/jphysiol.1978.sp012370
– volume: 414
  start-page: 813
  year: 2001
  ident: 2022031300065618700_B34
  article-title: Biochemistry and molecular cell biology of diabetic complications
  publication-title: Nature
  doi: 10.1038/414813a
– volume: 51
  start-page: 2997
  year: 2002
  ident: 2022031300065618700_B24
  article-title: Early, selective, and marked loss of sympathetic nerves from the islets of BioBreeder diabetic rats
  publication-title: Diabetes
  doi: 10.2337/diabetes.51.10.2997
– volume: 353
  start-page: 2643
  year: 2005
  ident: 2022031300065618700_B9
  article-title: Intensive diabetes treatment and cardiovascular disease in patients with type 1 diabetes
  publication-title: N Engl J Med
  doi: 10.1056/NEJMoa052187
– volume: 10
  start-page: 332
  year: 1989
  ident: 2022031300065618700_B14
  article-title: The contribution of the autonomic nervous system to changes of glucagon and insulin secretion during hypoglycemic stress
  publication-title: Endocr Rev
  doi: 10.1210/edrv-10-3-332
– volume: 153
  start-page: 1055
  year: 2012
  ident: 2022031300065618700_B20
  article-title: Minireview: the role of the autonomic nervous system in mediating the glucagon response to hypoglycemia
  publication-title: Endocrinology
  doi: 10.1210/en.2011-2040
– volume: 30
  start-page: 924
  year: 1987
  ident: 2022031300065618700_B53
  article-title: Counterregulation in type 2 (non-insulin-dependent) diabetes mellitus. Normal endocrine and glycaemic responses, up to ten years after diagnosis
  publication-title: Diabetologia
  doi: 10.1007/BF00295875
– volume: 182
  start-page: 171
  year: 1973
  ident: 2022031300065618700_B1
  article-title: Lack of glucagon response to hypoglycemia in diabetes: evidence for an intrinsic pancreatic alpha cell defect
  publication-title: Science
  doi: 10.1126/science.182.4108.171
– volume: 14
  start-page: 45
  year: 2011
  ident: 2022031300065618700_B44
  publication-title: Cell Metab
  doi: 10.1016/j.cmet.2011.05.008
– volume: 52
  start-page: 1246
  year: 1973
  ident: 2022031300065618700_B15
  article-title: Glucagon release induced by pancreatic nerve stimulation in the dog
  publication-title: J Clin Invest
  doi: 10.1172/JCI107292
– volume: 63
  start-page: 2369
  year: 2014
  ident: 2022031300065618700_B26
  article-title: The p75 neurotrophin receptor is required for the major loss of sympathetic nerves from islets under autoimmune attack
  publication-title: Diabetes
  doi: 10.2337/db13-0778
– volume: 329
  start-page: 977
  year: 1993
  ident: 2022031300065618700_B6
  article-title: The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus
  publication-title: N Engl J Med
  doi: 10.1056/NEJM199309303291401
– volume: 82
  start-page: 1538
  year: 1988
  ident: 2022031300065618700_B48
  article-title: Pancreatic noradrenergic nerves are activated by neuroglucopenia but not by hypotension or hypoxia in the dog. Evidence for stress-specific and regionally selective activation of the sympathetic nervous system
  publication-title: J Clin Invest
  doi: 10.1172/JCI113763
– volume: 52
  start-page: 2602
  year: 2009
  ident: 2022031300065618700_B25
  article-title: Loss of islet sympathetic nerves and impairment of glucagon secretion in the NOD mouse: relationship to invasive insulitis
  publication-title: Diabetologia
  doi: 10.1007/s00125-009-1494-5
– volume: 47
  start-page: 995
  year: 1998
  ident: 2022031300065618700_B19
  article-title: Autonomic mediation of glucagon secretion during hypoglycemia: implications for impaired alpha-cell responses in type 1 diabetes
  publication-title: Diabetes
  doi: 10.2337/diabetes.47.7.995
– volume: 7
  start-page: 988
  year: 2007
  ident: 2022031300065618700_B39
  article-title: Type 1 diabetes as a relapsing-remitting disease?
  publication-title: Nat Rev Immunol
  doi: 10.1038/nri2192
– volume: 9
  start-page: 750
  year: 2013
  ident: 2022031300065618700_B37
  article-title: Type 2 diabetes mellitus--an autoimmune disease?
  publication-title: Nat Rev Endocrinol
  doi: 10.1038/nrendo.2013.131
– volume: 50
  start-page: 217
  year: 2001
  ident: 2022031300065618700_B36
  article-title: The discovery of type 1 diabetes
  publication-title: Diabetes
  doi: 10.2337/diabetes.50.2.217
– volume: 155
  start-page: 173
  year: 2009
  ident: 2022031300065618700_B40
  article-title: Analysis of islet inflammation in human type 1 diabetes
  publication-title: Clin Exp Immunol
  doi: 10.1111/j.1365-2249.2008.03860.x
– volume: 11
  start-page: 649
  year: 2008
  ident: 2022031300065618700_B35
  article-title: Developmental axon pruning mediated by BDNF-p75NTR-dependent axon degeneration
  publication-title: Nat Neurosci
  doi: 10.1038/nn.2114
– ident: 2022031300065618700_B54
– volume: 372
  start-page: 1722
  year: 2015
  ident: 2022031300065618700_B7
  article-title: Intensive diabetes therapy and ocular surgery in type 1 diabetes
  publication-title: N Engl J Med
  doi: 10.1056/NEJMoa1409463
– volume: 44
  start-page: 1355
  year: 1995
  ident: 2022031300065618700_B55
  article-title: Clinical trials of diabetic neuropathy: past, present, and future
  publication-title: Diabetes
  doi: 10.2337/diab.44.12.1355
– volume: 46
  start-page: 801
  year: 1997
  ident: 2022031300065618700_B10
  article-title: Activation of autonomic nerves and the adrenal medulla contributes to increased glucagon secretion during moderate insulin-induced hypoglycemia in women
  publication-title: Diabetes
  doi: 10.2337/diab.46.5.801
– volume: 25
  start-page: 610
  year: 1995
  ident: 2022031300065618700_B30
  article-title: Metaiodobenzylguanidine imaging in diabetes mellitus: assessment of cardiac sympathetic denervation and its relation to autonomic dysfunction and silent myocardial ischemia
  publication-title: J Am Coll Cardiol
  doi: 10.1016/0735-1097(94)00459-4
– volume: 352
  start-page: 837
  year: 1998
  ident: 2022031300065618700_B33
  article-title: Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33)
  publication-title: Lancet
  doi: 10.1016/S0140-6736(98)07019-6
– volume: 15
  start-page: 127
  year: 2014
  ident: 2022031300065618700_B3
  article-title: Blunted glucagon but not epinephrine responses to hypoglycemia occurs in youth with less than 1 yr duration of type 1 diabetes mellitus
  publication-title: Pediatr Diabetes
  doi: 10.1111/pedi.12070
– reference: 6337896 - Diabetes. 1983 Feb;32(2):134-41
– reference: 7031230 - J Physiol. 1981 Jun;315:31-41
– reference: 690873 - J Physiol. 1978 Jul;280:25-35
– reference: 6491 - J Clin Invest. 1976 Jul;58(1):7-15
– reference: 19128359 - Clin Exp Immunol. 2009 Feb;155(2):173-81
– reference: 6341018 - Diabetes Care. 1983 Jan-Feb;6(1):95-9
– reference: 15958126 - J Peripher Nerv Syst. 2005 Jun;10(2):144-57
– reference: 2897940 - Diabetes. 1988 Apr;37(4):476-81
– reference: 25923552 - N Engl J Med. 2015 Apr 30;372(18):1722-33
– reference: 9736052 - Muscle Nerve. 1998 Oct;21(10):1246-55
– reference: 7589838 - Diabetes. 1995 Dec;44(12):1355-61
– reference: 22077236 - N Engl J Med. 2011 Dec 22;365(25):2366-76
– reference: 6111894 - Acta Physiol Scand. 1981 Jan;111(1):9-14
– reference: 12351439 - Diabetes. 2002 Oct;51(10):2997-3002
– reference: 22315452 - Endocrinology. 2012 Mar;153(3):1055-62
– reference: 4581053 - Science. 1973 Oct 12;182(4108):171-3
– reference: 4349486 - J Clin Invest. 1973 May;52(5):1246-59
– reference: 21723503 - Cell Metab. 2011 Jul 6;14(1):45-54
– reference: 17982429 - Nat Rev Immunol. 2007 Dec;7(12):988-94
– reference: 2883061 - Diabetologia. 1986 Dec;29(12):827-36
– reference: 21723498 - Cell Metab. 2011 Jul 6;14(1):5-6
– reference: 8366922 - N Engl J Med. 1993 Sep 30;329(14):977-86
– reference: 9133547 - Diabetes. 1997 May;46(5):801-7
– reference: 838846 - J Clin Endocrinol Metab. 1977 Mar;44(3):459-64
– reference: 25410245 - Handb Clin Neurol. 2014;126:579-602
– reference: 23266467 - Diabetes Metab. 2013 Feb;39(1):63-70
– reference: 3552240 - Cell Tissue Res. 1987 Apr;248(1):43-8
– reference: 641155 - J Clin Invest. 1978 Mar;61(3):781-9
– reference: 23992543 - Pediatr Diabetes. 2014 Mar;15(2):127-34
– reference: 9742976 - Lancet. 1998 Sep 12;352(9131):837-53
– reference: 18382462 - Nat Neurosci. 2008 Jun;11(6):649-58
– reference: 17684049 - J Clin Endocrinol Metab. 2007 Oct;92(10):4035-8
– reference: 19798480 - Diabetologia. 2009 Dec;52(12):2602-11
– reference: 11742414 - Nature. 2001 Dec 13;414(6865):813-20
– reference: 9176171 - Am J Physiol. 1997 May;272(5 Pt 1):E746-55
– reference: 6632773 - Lab Invest. 1983 Nov;49(5):538-52
– reference: 3297643 - Endocrinology. 1987 Jul;121(1):323-31
– reference: 8772469 - Am J Physiol. 1996 Jan;270(1 Pt 1):E20-6
– reference: 15793206 - Diabetes Care. 2005 Apr;28(4):956-62
– reference: 7860904 - J Am Coll Cardiol. 1995 Mar 1;25(3):610-8
– reference: 24608438 - Diabetes. 2014 Jul;63(7):2369-79
– reference: 2673755 - Endocr Rev. 1989 Aug;10(3):332-50
– reference: 23835371 - Nat Rev Endocrinol. 2013 Dec;9(12):750-5
– reference: 20876709 - Diabetes Care. 2010 Oct;33(10):2285-93
– reference: 2993084 - Diabetes. 1985 Sep;34(9):870-5
– reference: 11469712 - Diabetes Technol Ther. 2001 Spring;3(1):9-22
– reference: 7027713 - Acta Endocrinol (Copenh). 1981 Nov;98(3):402-6
– reference: 26581594 - Diabetes. 2016 Mar;65(3):719-31
– reference: 3183052 - J Clin Invest. 1988 Nov;82(5):1538-45
– reference: 9648820 - Diabetes. 1998 Jul;47(7):995-1005
– reference: 16371630 - N Engl J Med. 2005 Dec 22;353(25):2643-53
– reference: 3325324 - Diabetologia. 1987 Dec;30(12):924-9
– reference: 4785433 - J Clin Endocrinol Metab. 1973 Sep;37(3):479-81
– reference: 11272129 - Diabetes. 2001 Feb;50(2):217-26
– reference: 24217518 - Nat Rev Neurol. 2013 Dec;9(12):668-76
– reference: 12876072 - Am J Physiol Endocrinol Metab. 2003 Nov;285(5):E1047-54
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Snippet In humans, the glucagon response to moderate-to-marked insulin-induced hypoglycemia (IIH) is largely mediated by the autonomic nervous system. Because this...
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StartPage 2322
SubjectTerms Adolescent
Adult
Autonomic Nervous System - metabolism
Autonomic Nervous System - pathology
Autonomic Nervous System - physiopathology
Child
Diabetes
Diabetes Mellitus, Type 1 - metabolism
Diabetes Mellitus, Type 1 - pathology
Diabetes Mellitus, Type 1 - physiopathology
Diabetes Mellitus, Type 2 - metabolism
Diabetes Mellitus, Type 2 - pathology
Diabetes Mellitus, Type 2 - physiopathology
Female
Glucagon - metabolism
Humans
Hypoglycemia
Hypoglycemia - metabolism
Hypoglycemia - pathology
Hypoglycemia - physiopathology
Immunohistochemistry
Insulin
Islet Studies
Islets of Langerhans - metabolism
Islets of Langerhans - pathology
Islets of Langerhans - physiopathology
Male
Middle Aged
Nervous system
Pancreas - metabolism
Pancreas - pathology
Pancreas - physiopathology
Sympathetic Nervous System - metabolism
Sympathetic Nervous System - pathology
Sympathetic Nervous System - physiopathology
Young Adult
Title Human Type 1 Diabetes Is Characterized by an Early, Marked, Sustained, and Islet-Selective Loss of Sympathetic Nerves
URI https://www.ncbi.nlm.nih.gov/pubmed/27207540
https://www.proquest.com/docview/1807268572
https://www.proquest.com/docview/1807274897
https://www.proquest.com/docview/1815702315
https://pubmed.ncbi.nlm.nih.gov/PMC4955989
Volume 65
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