Scientists have generated patient-specific beta cells, or insulin-producing cells, that accurately reflect the features of maturity-onset diabetes of the young.
Jacob Blumenthal's insight:
Abstract: Diabetes is a disorder characterized by loss of β cell mass and/or β cell function, leading to deficiency of insulin relative to metabolic need. To determine whether stem cell–derived β cells recapitulate molecular-physiological phenotypes of a diabetic subject, we generated induced pluripotent stem cells (iPSCs) from subjects with maturity-onset diabetes of the young type 2 (MODY2), which is characterized by heterozygous loss of function of the gene encoding glucokinase (GCK). These stem cells differentiated into β cells with efficiency comparable to that of controls and expressed markers of mature β cells, including urocortin-3 and zinc transporter 8, upon transplantation into mice. While insulin secretion in response to arginine or other secretagogues was identical to that in cells from healthy controls, GCK mutant β cells required higher glucose levels to stimulate insulin secretion. Importantly, this glucose-specific phenotype was fully reverted upon gene sequence correction by homologous recombination. Our results demonstrate that iPSC-derived β cells reflect β cell–autonomous phenotypes of MODY2 subjects, providing a platform for mechanistic analysis of specific genotypes on β cell function.
Researchers derived induced pluripotent stem (iPS) cells from skin cells taken from patients with a rare form of diabetes -- Wolfram syndrome. Then they differentiated these iPS cells into beta-like cells, and found that the derived cells failed to secrete insulin due to protein-folding, or endoplasmic reticulum (ER) stress. By adding 4-phenyl butyric acid, the cells regain the ability to secrete insulin.
This paper is a good example to the ability to use iPS cells as iin-vitro disease models, to gain insight into disease-related molecular mechanisms and to screen for potential drugs.
In a paper, published in Development journal, researchers from the Danish Stem Cell Centre have shown that they can culture mouse pancreatic cells into expanded, branched structures in a 3D culture.
By manipulating the medium composition they generated either hollow spheres, which are mainly composed of pancreatic progenitors, or complex organoids that spontaneously undergo pancreatic morphogenesis and differentiation.
Manipulation and improvement of culture and expansion techniques
could lead to a more efficient and developed method of creating insulin-releasing beta cells, which will eventually be used for cell therapy of diabetes.
Hormone found by Harvard's Melton and Yi has the potential to change the way Type 2 diabetes is treated
Jacob Blumenthal's insight:
This is an exciting discovery! In adults, pancreatic β cells are generated primarily by self-duplication. The researchers report on a mouse model of insulin resistance that induces dramatic pancreatic β cell proliferation and β cell mass expansion. Using this model, the researchers identified a hormone, betatrophin, that is primarily expressed in liver and fat. The discovery of the betatrophin hormone may lead to the development of therapy to diabetes in the future.
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