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Aberrant bone marrow-derived microglia in the hypothalamus may dysregulate appetite in diabetes
Ist Teil von
Biochemical and biophysical research communications, 2023-11, Vol.682, p.132-137
Ort / Verlag
Elsevier Inc
Erscheinungsjahr
2023
Quelle
Alma/SFX Local Collection
Beschreibungen/Notizen
Bone marrow derived cells (BMDCs) migrate into the hypothalamus, where those cells give rise to microglia to regulate food intake. Given the fact that diabetes functionally impairs BMDCs, we hypothesized that diabetic microglia would fail to exhibit physiological function, accounting for hyperphagia in diabetes. To examine the role of BMDCs, total bone marrow cells from GFP transgenic mice were transplanted into wild type mice in which diabetes was induced by streptozotocin. We first confirmed that bone marrow transplantation could be utilized to examine BMDCs in the brain parenchyma as GFP positive cells could engraft the brain parenchyma and give rise to microglia even when the BBB was intact in the recipient mice. While diabetic mice manifested hyperphagia, BMDCs were in smaller number in the hypothalamus with less response to fasting in the brain parenchyma compared to nondiabetic mice. This finding was also confirmed by examining nondiabetic chimera mice in which BMDCs were diabetic. Those mice also exhibited less response of BMDCs in response to fasting. In conclusion, diabetic BMDCs had less response of microglia to fasting, perhaps accounting for diabetic hyperphagia.
•Appetite dysregulation occurs in diabetes, but the cause is unknown.•The paraventricular nucleus of the hypothalamus is important in appetite regulation.•We investigated the behavior of bone marrow-derived microglia in the paraventricular nucleus of diabetic mice in the presence or absence of feeding.•In nondiabetic mice, the number of these cells increased with fasting, but in diabetic mice they decreased and did not respond to fasting.•Abnormalities in bone marrow-derived microglia are thought to be an important cause of appetite dysregulation in diabetes.
Sprache
Englisch
Identifikatoren
ISSN: 0006-291X
eISSN: 1090-2104
DOI: 10.1016/j.bbrc.2023.09.083
Titel-ID: cdi_proquest_miscellaneous_2874837263
Format
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