Insulin resistance alters islet morphology in nondiabetic humans

Research output: Contribution to journal › Journal article › Research › peer-review

Standard

Insulin resistance alters islet morphology in nondiabetic humans. / Mezza, Teresa; Muscogiuri, Giovanna; Sorice, Gian Pio; Clemente, Gennaro; Hu, Jiang; Pontecorvi, Alfredo; Holst, Jens Juul; Giaccari, Andrea; Kulkarni, Rohit N.

In: Diabetes, Vol. 63, No. 3, 03.2014, p. 994-1007.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Mezza, T, Muscogiuri, G, Sorice, GP, Clemente, G, Hu, J, Pontecorvi, A, Holst, JJ, Giaccari, A & Kulkarni, RN 2014, 'Insulin resistance alters islet morphology in nondiabetic humans', Diabetes, vol. 63, no. 3, pp. 994-1007. https://doi.org/10.2337/db13-1013

APA

Mezza, T., Muscogiuri, G., Sorice, G. P., Clemente, G., Hu, J., Pontecorvi, A., Holst, J. J., Giaccari, A., & Kulkarni, R. N. (2014). Insulin resistance alters islet morphology in nondiabetic humans. Diabetes, 63(3), 994-1007. https://doi.org/10.2337/db13-1013

Vancouver

Mezza T, Muscogiuri G, Sorice GP, Clemente G, Hu J, Pontecorvi A et al. Insulin resistance alters islet morphology in nondiabetic humans. Diabetes. 2014 Mar;63(3):994-1007. https://doi.org/10.2337/db13-1013

Author

Mezza, Teresa ; Muscogiuri, Giovanna ; Sorice, Gian Pio ; Clemente, Gennaro ; Hu, Jiang ; Pontecorvi, Alfredo ; Holst, Jens Juul ; Giaccari, Andrea ; Kulkarni, Rohit N. / Insulin resistance alters islet morphology in nondiabetic humans. In: Diabetes. 2014 ; Vol. 63, No. 3. pp. 994-1007.

Bibtex

@article{6f03a57cf9184f4c80df5378fb33da2d,
title = "Insulin resistance alters islet morphology in nondiabetic humans",
abstract = "Type 2 diabetes is characterized by poor glucose uptake in metabolic tissues and manifests when insulin secretion fails to cope with worsening insulin resistance. In addition to its effects on skeletal muscle, liver, and adipose tissue metabolism, it is evident that insulin resistance also affects pancreatic β-cells. To directly examine the alterations that occur in islet morphology as part of an adaptive mechanism to insulin resistance, we evaluated pancreas samples obtained during pancreatoduodenectomy from nondiabetic subjects who were insulin-resistant or insulin-sensitive. We also compared insulin sensitivity, insulin secretion, and incretin levels between the two groups. We report an increased islet size and an elevated number of β- and α-cells that resulted in an altered β-cell-to-α-cell area in the insulin- resistant group. Our data in this series of studies suggest that neogenesis from duct cells and transdifferentiation of α-cells are potential contributors to the β-cell compensatory response to insulin resistance in the absence of overt diabetes.",
keywords = "Adult, Aged, Female, Glucagon-Like Peptide 1, Glucagon-Secreting Cells, Humans, Hyperplasia, Insulin Resistance, Insulin-Secreting Cells, Islets of Langerhans, Male, Middle Aged, Pancreatectomy",
author = "Teresa Mezza and Giovanna Muscogiuri and Sorice, {Gian Pio} and Gennaro Clemente and Jiang Hu and Alfredo Pontecorvi and Holst, {Jens Juul} and Andrea Giaccari and Kulkarni, {Rohit N}",
year = "2014",
month = mar,
doi = "10.2337/db13-1013",
language = "English",
volume = "63",
pages = "994--1007",
journal = "Diabetes",
issn = "0012-1797",
publisher = "American Diabetes Association",
number = "3",

}

RIS

TY - JOUR

T1 - Insulin resistance alters islet morphology in nondiabetic humans

AU - Mezza, Teresa

AU - Muscogiuri, Giovanna

AU - Sorice, Gian Pio

AU - Clemente, Gennaro

AU - Hu, Jiang

AU - Pontecorvi, Alfredo

AU - Holst, Jens Juul

AU - Giaccari, Andrea

AU - Kulkarni, Rohit N

PY - 2014/3

Y1 - 2014/3

N2 - Type 2 diabetes is characterized by poor glucose uptake in metabolic tissues and manifests when insulin secretion fails to cope with worsening insulin resistance. In addition to its effects on skeletal muscle, liver, and adipose tissue metabolism, it is evident that insulin resistance also affects pancreatic β-cells. To directly examine the alterations that occur in islet morphology as part of an adaptive mechanism to insulin resistance, we evaluated pancreas samples obtained during pancreatoduodenectomy from nondiabetic subjects who were insulin-resistant or insulin-sensitive. We also compared insulin sensitivity, insulin secretion, and incretin levels between the two groups. We report an increased islet size and an elevated number of β- and α-cells that resulted in an altered β-cell-to-α-cell area in the insulin- resistant group. Our data in this series of studies suggest that neogenesis from duct cells and transdifferentiation of α-cells are potential contributors to the β-cell compensatory response to insulin resistance in the absence of overt diabetes.

AB - Type 2 diabetes is characterized by poor glucose uptake in metabolic tissues and manifests when insulin secretion fails to cope with worsening insulin resistance. In addition to its effects on skeletal muscle, liver, and adipose tissue metabolism, it is evident that insulin resistance also affects pancreatic β-cells. To directly examine the alterations that occur in islet morphology as part of an adaptive mechanism to insulin resistance, we evaluated pancreas samples obtained during pancreatoduodenectomy from nondiabetic subjects who were insulin-resistant or insulin-sensitive. We also compared insulin sensitivity, insulin secretion, and incretin levels between the two groups. We report an increased islet size and an elevated number of β- and α-cells that resulted in an altered β-cell-to-α-cell area in the insulin- resistant group. Our data in this series of studies suggest that neogenesis from duct cells and transdifferentiation of α-cells are potential contributors to the β-cell compensatory response to insulin resistance in the absence of overt diabetes.

KW - Adult

KW - Aged

KW - Female

KW - Glucagon-Like Peptide 1

KW - Glucagon-Secreting Cells

KW - Humans

KW - Hyperplasia

KW - Insulin Resistance

KW - Insulin-Secreting Cells

KW - Islets of Langerhans

KW - Male

KW - Middle Aged

KW - Pancreatectomy

U2 - 10.2337/db13-1013

DO - 10.2337/db13-1013

M3 - Journal article

C2 - 24215793

VL - 63

SP - 994

EP - 1007

JO - Diabetes

JF - Diabetes

SN - 0012-1797

IS - 3

ER -

ID: 117853024