Insulin resistance alters islet morphology in nondiabetic humans
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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
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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