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Inadequate ß-cell mass is essential for the pathogenesis of type 2 diabetes.
Weir, Gordon C; Gaglia, Jason; Bonner-Weir, Susan.
Affiliation
  • Weir GC; Section on Islet Cell and Regenerative Biology, Joslin Diabetes Center, Harvard Medical School, Boston, MA, USA. Electronic address: gordon.weir@joslin.harvard.edu.
  • Gaglia J; Section on Immunobiology, Joslin Diabetes Center, Harvard Medical School, Boston, MA, USA.
  • Bonner-Weir S; Section on Islet Cell and Regenerative Biology, Joslin Diabetes Center, Harvard Medical School, Boston, MA, USA.
Lancet Diabetes Endocrinol ; 8(3): 249-256, 2020 03.
Article in En | MEDLINE | ID: mdl-32006519
ABSTRACT
For patients with type 1 diabetes, it is accepted among the scientific community that there is a marked reduction in ß-cell mass; however, with type 2 diabetes, there is disagreement as to whether this reduction in mass occurs in every case. Some have argued that ß-cell mass in some patients with type 2 diabetes is normal and that the cause of the hyperglycaemia in these patients is a functional abnormality of insulin secretion. In this Personal View, we argue that a deficient ß-cell mass is essential for the development of type 2 diabetes. The main point is that there are enormous (≥10 fold) variations in insulin sensitivity and insulin secretion in the general population, with a very close correlation between these two factors for any individual. Although ß-cell mass cannot be accurately measured in living patients, it is highly likely that it too is highly correlated with insulin sensitivity and secretion. Thus, our argument is that a person with type 2 diabetes can have a ß-cell mass that is the same as a person without type 2 diabetes, but because they are insulin resistant, the mass is inadequate and responsible for their diabetes. Because the abnormal insulin secretion of diabetes is caused by dysglycaemia and can be largely reversed with glycaemic control, it is a less serious problem than the reduction in ß-cell mass, which is far more difficult to restore.
Subject(s)

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Diabetes Mellitus, Type 2 / Insulin-Secreting Cells / Insulin Secretion Type of study: Etiology_studies Limits: Humans Language: En Journal: Lancet Diabetes Endocrinol Year: 2020 Document type: Article

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Diabetes Mellitus, Type 2 / Insulin-Secreting Cells / Insulin Secretion Type of study: Etiology_studies Limits: Humans Language: En Journal: Lancet Diabetes Endocrinol Year: 2020 Document type: Article