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Osteoblast-derived intraflagellar transport 140 suppresses insulin sensitivity I

ABSTRACT: Hyperglycemia-induced damage to bone formations and function has been recognized.However, as the largest connective tissue organ, whether bone and osteocytes in turn regulate blood sugar and insulin sensitivity has not been addressed. Here we identified a novel protein termed intraflagellar transport 140 with functional importance in regulating osteogenesis, which is also related to the osteoblastic insulin sensitivity. We established Ift140 osteoblastic conditional knockout mice model, and found that blood glucose metabolism could be regulated through osteoblastic IFT140 interacting with O-GlcNAc transferase to regulate insulin signaling. The discovery provides new insight for two-way regulation between bone and glucose metabolism, and also exploring potential new target for blood glucose interventions.

ORGANISM(S): Mus musculus

PROVIDER: GSE178548 | GEO | 2021/06/24

REPOSITORIES: GEO

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Osteoblast-derived intraflagellar transport 140 suppresses insulin sensitivity II

Project description:Hyperglycemia-induced damage to bone formations and function has been recognized.However, as the largest connective tissue organ, whether bone and osteocytes in turn regulate blood sugar and insulin sensitivity has not been addressed. Here we identified a novel protein termed intraflagellar transport 140 with functional importance in regulating osteogenesis, which is also related to the osteoblastic insulin sensitivity. We established Ift140 osteoblastic conditional knockout mice model, and found that blood glucose metabolism could be regulated through osteoblastic IFT140 interacting with O-GlcNAc transferase to regulate insulin signaling. The discovery provides new insight for two-way regulation between bone and glucose metabolism, and also exploring potential new target for blood glucose interventions.

2021-06-24 | GSE178558 | GEO

Osteoblast-derived intraflagellar transport 140 suppresses insulin sensitivity

Project description:Osteoblast-derived intraflagellar transport 140 suppresses insulin sensitivity

| PRJNA739651 | ENA

Osteoblast-derived intraflagellar transport 140 suppresses insulin sensitivity I

Project description:Osteoblast-derived intraflagellar transport 140 suppresses insulin sensitivity I

| PRJNA739643 | ENA

Osteoblast-derived intraflagellar transport 140 suppresses insulin sensitivity II

Project description:Osteoblast-derived intraflagellar transport 140 suppresses insulin sensitivity II

| PRJNA739660 | ENA

Expression data from NPY Y1R-deficient osteoblastic cells

Project description:NPY signalling via osteoblastic Y1 receptors has been shown to control bone mass but also contributes significantly to the control of whole-body insulin secretion and glucose homeostasis in mice through the release of novel factor(s) which are different from the previously implicated osteocalcin. We used microarrays to identify novel endocrine factors regulated by Y1 receptors and involved in the regulation of bone mass and whole-body homeostasis.

2018-05-16 | GSE114469 | GEO

Insulin receptor signaling in osteoblasts regulates postnatal bone acquisition and body composition

Project description:Global energy balance in mammals is controlled by the actions of circulating hormones that coordinate fuel production and utilization in metabolically active tissues. Bone-derived osteocalcin, in its undercarboxylated, hormonal form, regulates fat deposition and is a potent insulin secretagogue. Here, we show that insulin receptor (IR) signaling in osteoblasts controls osteoblast development and osteocalcin expression by suppressing the Runx2 inhibitor Twist-2. Mice lacking IR in osteoblasts have low circulating undercarboxylated osteocalcin and reduced bone acquisition due to decreased bone formation and deficient numbers of osteoblasts. With age, these mice develop marked peripheral adiposity and hyperglycemia accompanied by severe glucose intolerance and insulin resistance. The metabolic abnormalities in these mice are improved by infusion of exogenous under-carboxylated osteocalcin. These results indicate the existence of a bone-pancreas endocrine loop through which insulin signaling in the osteoblast ensures osteoblast differentiation and stimulates osteocalcin production, which in turn regulates insulin sensitivity and pancreatic insulin secretion to control glucose homeostasis. We used microarrays to detail the global gene expression changes in response to insulin acting through insulin receptor in osteoblasts and identified distinct genes specifically involved in bone remodeling process. 4 groups and 3 time points (0h as a control, 6h, 12h, and 24h)

2010-05-27 | E-GEOD-21710 | biostudies-arrayexpress

Osteoblast-derived intraflagellar transport 140 suppresses insulin sensitivity

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-06-24 | GSE178561 | GEO

Insulin receptor signaling in osteoblasts regulates postnatal bone acquisition and body composition

2010-05-07 | GSE21710 | GEO

Impact of Preoperative Oral Branched-chain Amino Acids on Reducing Postoperative Insulin Resistance.

Project description:Postoperative insulin resistance refers to the phenomenon that the body’s glucose uptake stimulated by insulin is reduced due to stress effects such as trauma or the inhibitory effect of insulin on liver glucose output is weakened after surgery. There is a clear link between postoperative insulin resistance and poor perioperative prognosis. Therefore, exploring interventions to reduce postoperative stress insulin resistance, stabilize postoperative blood glucose, and reduce postoperative complications are clinical problems that need to be solved urgently. In recent years, research on branched-chain amino acids and metabolic diseases has become a hot spot. Studies have found that in the rat model, preoperatively given a high branched-chain amino acid diet can inhibit postoperative insulin resistance and stabilize blood glucose levels. This research plan is to try to add branched-chain amino acids before surgery to observe the occurrence of postoperative insulin resistance in patients.

| 2744698 | ecrin-mdr-crc

Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and 2.5ppm iAs Treated Mouse Gastrocnemius Muscle Transcriptomes

Project description:Inorganic arsenic (iAs) is a widespread environmental toxin. In addition to being a human carcinogen, its effect on systemic glucose metabolism has started to gain recognition recently. However, its in vivo effect on insulin sensitivity is not clear. Here we use mouse models to dissect the dose-dependent effects of iAs in glucose metabolism. We found that a low-dose exposure (0.25 ppm iAs in drinking water) caused glucose intolerance in adult male C57BL/6 mice, likely by disrupting glucose-induced insulin secretion without affecting peripheral insulin sensitivity. However, a higher-dose exposure (2.5 ppm iAs) has diminished effects on glucose tolerance despite disrupted pancreatic insulin secretion. We performed hyperinsulinemic euglycemic clamp, the gold standard analysis of systemic insulin sensitivity, and found that the 2.5 ppm iAs enhanced systemic insulin sensitivity by simultaneously enhancing insulin-stimulated glucose uptake in skeletal muscles and insulin-mediated suppression of endogenous glucose production. RNA-seq analysis of muscles revealed that 2.5 ppm iAs regulated expression of many genes involved in the metabolism of fatty acids, pyruvate, and amino acids. These findings suggest that iAs has distinct effects on distinct metabolic tissues at different dose thresholds, which could help reconcile some of the conflicting epidemiological results. The study shed light on the complex interactions between an environmental factor and the systemic glucose metabolism.

2018-11-16 | GSE122566 | GEO

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