Osteocalcin protects islet identity in low-density lipoprotein receptor knockout mice on high-fat diet

内分泌学 内科学 小岛 胰岛素 骨钙素 胰岛素原 胰岛素受体 医学 高胰岛素血症 生物 胰岛素抵抗 生物化学 碱性磷酸酶
作者
Christine A. Beamish,Yoon K. Lee,A. Osama Gaber,Priyanka Chanana,Edward A. Graviss,Małgorzata Kloc,M. Waleed Gaber,Willa A. Hsueh,Omaima Sabek
出处
期刊:Journal of Endocrinology [Bioscientifica]
卷期号:261 (1)
标识
DOI:10.1530/joe-23-0352
摘要

Metabolic syndrome (MetS) is an increasing global health threat and strong risk factor for type 2 diabetes (T2D). MetS causes both hyperinsulinemia and islet size overexpansion, and pancreatic β-cell failure impacts insulin and proinsulin secretion, mitochondrial density, and cellular identity loss. The low-density lipoprotein receptor knockout (LDLr-/-) model combined with high-fat diet (HFD) has been used to study alterations in multiple organs, but little is known about the changes to β-cell identity resulting from MetS. Osteocalcin (OC), an insulin-sensitizing protein secreted by bone, shows promising impact on β-cell identity and function. LDLr-/- mice at 12 months were fed chow or HFD for 3 months ± 4.5 ng/h OC. Islets were examined by immunofluorescence for alterations in nuclear Nkx6.1 and PDX1 presence, insulin-glucagon colocalization, islet size and %β-cell and islet area by insulin and synaptophysin, and mitochondria fluorescence intensity by Tomm20. Bone mineral density (BMD) and %fat changes were examined by Piximus Dexa scanning. HFD-fed mice showed fasting hyperglycemia by 15 months, increased weight gain, %fat, and fasting serum insulin and proinsulin; concurrent OC treatment mitigated weight increase and showed lower proinsulin-to-insulin ratio, and higher BMD. HFD increased %β and %islet area, while simultaneous OC-treatment with HFD was comparable to chow-fed mice. Significant reductions in nuclear PDX1 and Nkx6.1 expression, increased insulin-glucagon colocalization, and reduction in β-cell mitochondria fluorescence intensity were noted with HFD, but largely prevented with OC administration. OC supplementation here suggests a benefit to β-cell identity in LDLr-/- mice and offers intriguing clinical implications for countering metabolic syndrome.
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