α- or β-Adrenergic blockade does not affect transplanted islet cell responses to hypoglycemia in type 1 diabetes-Reference-Cited by-同舟云学术

α- or β-Adrenergic blockade does not affect transplanted islet cell responses to hypoglycemia in type 1 diabetes

Published:2024-09-01 Issue:3 Volume:327 Page:E290-E301
ISSN:0193-1849
Container-title:American Journal of Physiology-Endocrinology and Metabolism
language:en
Short-container-title:American Journal of Physiology-Endocrinology and Metabolism

Author:

Rickels Michael R.¹^ORCID,Bellin Melena D.²^ORCID,Stefanovski Darko³^ORCID,Peleckis Amy J.¹,Dalton-Bakes Cornelia¹,Markmann Eileen¹,Nguyen Huong-Lan¹,Townsend Raymond R.⁴^ORCID,Hering Bernhard J.⁵,Naji Ali⁶

Affiliation:

1. Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, United States

2. Division of Pediatric Endocrinology, Department of Pediatrics, University of Minnesota, Minneapolis, Minnesota, United States

3. Department of Biostatistics, University of Pennsylvania School of Veterinary Medicine, Kennett Square, Pennsylvania, United States

4. Division of Nephrology and Hypertension, Department of Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, United States

5. Schulze Diabetes Institute, Department of Surgery, University of Minnesota, Minneapolis, Minnesota, United States

6. Division of Transplant Surgery, Department of Surgery, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, United States

Abstract

Whether adrenergic input to islets is necessary for glucose homeostasis in humans is debated. Here, the adrenergic contribution to intrahepatically transplanted islet cell responses to hypoglycemia in individuals with type 1 diabetes was investigated through α- or β-adrenergic receptor blockade during hyperinsulinemic euglycemic-hypoglycemic clamps. Neither α- nor β-adrenergic blockage affected the suppression of endogenous insulin or activation of glucagon secretion, suggesting that sympathetic reinnervation of islet grafts is not required for posttransplant defense against hypoglycemia.

Funder

HHS | NIH | National Center for Advancing Translational Sciences

HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases

Publisher

American Physiological Society

Link

https://journals.physiology.org/doi/pdf/10.1152/ajpendo.00002.2024

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3. Restoration of Glucose Counterregulation by Islet Transplantation in Long-standing Type 1 Diabetes

4. Long-Term Improvement in Glucose Control and Counterregulation by Islet Transplantation for Type 1 Diabetes

5. Defective Glucagon Secretion During Hypoglycemia After Intrahepatic But Not Nonhepatic Islet Autotransplantation