Scholars map primate islet cell aging molecules

30 years, with the aging of the population, the incidence of diabetes in China has risen sharply.
However, the composition of islet cells is highly heterogeneic, containing a variety of cell types that secrete different types of hormones, while sample acquisition is technically difficult and ethically limited, which greatly restricts the mechanism of primate islet cell aging.
A study published in the National Science Review on June 10 systematically mapped high-precision single-cell transcription of islet aging in non-human primates, revealing that protein-stabilized imbalances are key features and molecular drivers of islet β cell aging. The study was carried out by
Jing, Liu Guanghui, a researcher at the
Institute of Animals, Zhang Weihui, a researcher at the
Beijing Genomics Research Institute, and Professor Tang Fuhui of Peking University.
" study revealed for the first time in the world the single-cell transcriptional map of non-primate islet aging, which provides a potential intervention target for slowing islet aging and restoring the glucose tolerance of elderly individuals, and may provide new ideas for the prevention and treatment of diabetes. Qu Jing, co-author of the article, said.
using high-precision single-cell transcription group sequencing techniques, the researchers described the gene expression characteristics of islet cells such as α cells, β cells, δ cells and PP cells, and identified a series of new molecular markers.
Through aging transcription noise analysis, aging marker analysis, and a joint analysis with databases such as Aging/Diabetes, α and β cells were more prone to abnormal changes in the aging process than other cell types, and they analyzed the changes.
found that aging causes severe damage β protein stability in our cells, " he said. The specific performance is that in the β cells of the elderly individual, the protein aggregation experience abnormal accumulation, the expression of ATF6 and IRE1 signaling path in the unfolded protein response path, especially the expression of the endosperm molecular companion protein HSP90B1 in the elderly individual β cells. Zhang Weixuan, another co-author of the article, said.
further studies have shown that over-expression of HSP90B1 in β cells can lead to reduced insulin secretion under high glucose stimulation, suggesting that an increase in the ageing expression of HSP90B1 in β cells may be the driving force behind the decrease in sugar tolerance in older adults. (Source: Liu Runan, China Science Journal)
relevant paper information: