Effect of Glucagon-like Peptide-1 on the Differentiation of Adipose-derived Stem Cells into Osteoblasts and Adipocytes

Lee, Hye Min; Joo, Bo Sun; Lee, Chang Hoon; Kim, Heung Yeol; Ock, Ji Hoon; Lee, Young Seok

doi:10.6118/jmm.2015.21.2.93

Cited by 35 publications

(29 citation statements)

References 40 publications

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“…Consequently, positive neuropathological effects such as improvement in scholastic skills, memory were shown. In this mechanism, up-regulated interleukin-10 and neurotrophic factors, which both are neuroprotective, were shown 8. Also, level of amyloid beta and C-protein that destroying brain cells were significantly decreased due to the effect of stem cell administration, and this is because toxoprotein proteolytic enzyme were increased.…”

Section: Cell Therapy Developmentmentioning

confidence: 94%

Cell Therapy Products in Alzheimer Disease

et al. 2017

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We are rapidly becoming an aging society, with the ongoing increase in challenges of the elderly. The age-related cognitive decline in accordance with aging society is of major importance in public health. Recent studies have proved the impacts of sex-steroid hormone on the brain; compliant with aging, menopause and decrease in estrogen have an effect on the occurrence and prevention of Alzheimer's disease. A new hypothesis states that Alzheimer's disease is a postmenopausal dementia, and is a negative form of estrogen deficiency. In this review article, we reckoned the cause of postmenopausal Alzheimer's disease. We further investigated new cell therapies for postmenopausal Alzheimer's disease, which are under development in some pharmaceutical companies. One remedy is cell therapy that inhibits the amyloid beta formation, and the other is the umbilical cord blood derived mesenchymal stem cell therapy.

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Section: Cell Therapy Developmentmentioning

confidence: 94%

Cell Therapy Products in Alzheimer Disease

et al. 2017

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“…GIPR indicated but not confirmed GIP protected osteoblast-like cells from apoptosis in a dose-dependent manner Sanz [21] Human mesenchymal stem cells GLP-1 (10 nM) GLP-1R expressed in human mesenchymal stem cells GLP-1 promoted differentiation and decreased apoptosis of human mesenchymal stem cells GLP-1 inhibited adipocyte differentiation, partly through decreasing PPARc Jeon [22] Human adipose-derived stem cells GLP-1R expressed in human adipose-derived stem cells Lee [23] Human adipose-derived stem cells GLP-1 (10 and 100 nM) GLP-1 treatment increased alkaline phosphatase expression (at 100 nM GLP-1). GLP-1 decreased adipogenic differentiation of human adipose-derived stem cells (at 100 nM).…”

Section: Referencesmentioning

confidence: 99%

Effects of gastric inhibitory polypeptide, glucagon‐like peptide‐1 and glucagon‐like peptide‐1 receptor agonists on Bone Cell Metabolism

Hansen

Tencerová

Frølich

et al. 2017

Basic Clin Pharma Tox

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Abstract:The relationship between gut and skeleton is increasingly recognized as part of the integrated physiology of the whole organism. The incretin hormones gastric inhibitory polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are secreted from the intestine in response to nutrient intake and exhibit several physiological functions including regulation of islet hormone secretion and glucose levels. A number of GLP-1 receptor agonists (GLP-1RAs) are currently used in treatment of type 2 diabetes and obesity. However, GIP and GLP-1 cognate receptors are widely expressed suggesting that incretin hormones mediate effects beyond control of glucose homeostasis, and reports on associations between incretin hormones and bone metabolism have emerged. The aim of this MiniReview was to provide an overview of current knowledge regarding the in vivo and in vitro effects of GIP and GLP-1 on bone metabolism. We identified a total of 30 pre-clinical and clinical investigations of the effects of GIP, GLP-1 and GLP-1RAs on bone turnover markers, bone mineral density (BMD), bone microarchitecture and fracture risk. Studies conducted in cell cultures and rodents demonstrated that GIP and GLP-1 play a role in regulating skeletal homeostasis, with preclinical data suggesting that GIP inhibits bone resorption whereas GLP-1 may promote bone formation and enhance bone material properties. These effects are not corroborated by clinical studies. While there is evidence of effects of GIP and GLP-1 on bone metabolism in pre-clinical investigations, clinical trials are needed to clarify whether similar effects are present and clinically relevant in humans.Bone remodelling is the regenerative mechanism that maintains the skeletal health and biomechanical competence through resorption of bone by osteoclasts and formation of new bone by osteoblasts. These processes are highly co-ordinated and under the influence of several hormonal factors [1].Incretin hormones encompass a group of hormones characterized by their ability to enhance insulin secretion in response to intake of nutrients, such as glucose and fat. The most important incretin hormones are gastric inhibitory polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) [2]. Both of these hormones interact with cognate receptors, which are widely expressed in human tissues: the GIP receptor (GIPR) is expressed in pancreas, central nervous system, thyroid as well as adipose tissue [3], and the GLP-1 receptor (GLP-1R) is expressed in the kidney, stomach, duodenum, central nervous system and pancreas [4]. Both the GIP and the GLP-1 receptors are 7-transmembrane proteins, and activation of these receptors by binding of either GIP or GLP-1 increases intracellular levels of cyclic adenosine monophosphate (cAMP) and Ca 2+ [5].Gastric inhibitory polypeptide and GLP-1 are secreted from enteroendocrine cells of the small intestine. Once secreted, GLP-1 binds to the GLP-1 receptors expressed on pancreatic b-cells, leading to a glucose-dependent insulin secretion but the effect is short-lived as GLP...

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“…Glucagon-like peptide-1 (GLP-1) is an intestinal hormone that plays an essential role in the regulation of glucose homeostasis. In human adipose-derived stromal stem cells, GLP-1 stimulated osteoblastic cell differentiation and suppressed adipogenesis [44]. In these cells, inhibiting ERK reversed the anti-adipogenic effect of GLP-1 [44].…”

Section: Glucagon-like Peptide-1mentioning

confidence: 99%

Insulin Signaling in Bone Marrow Adipocytes

Tencerová

Okla

Kassem

2019

Curr Osteoporos Rep

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Purpose of Review The goal of this review is to discuss the role of insulin signaling in bone marrow adipocyte formation, metabolic function, and its contribution to cellular senescence in relation to metabolic bone diseases. Recent Findings Insulin signaling is an evolutionally conserved signaling pathway that plays a critical role in the regulation of metabolism and longevity. Bone is an insulin-responsive organ that plays a role in whole body energy metabolism. Metabolic disturbances associated with obesity and type 2 diabetes increase a risk of fragility fractures along with increased bone marrow adiposity. In obesity, there is impaired insulin signaling in peripheral tissues leading to insulin resistance. However, insulin signaling is maintained in bone marrow microenvironment leading to hypermetabolic state of bone marrow stromal (skeletal) stem cells associated with accelerated senescence and accumulation of bone marrow adipocytes in obesity. Summary This review summarizes current findings on insulin signaling in bone marrow adipocytes and bone marrow stromal (skeletal) stem cells and its importance for bone and fat metabolism. Moreover, it points out to the existence of differences between bone marrow and peripheral fat metabolism which may be relevant for developing therapeutic strategies for treatment of metabolic bone diseases.with enhanced insulin sensitivity, glucose uptake, and oxidative phosphorylation. This metabolic phenotype of BMSC in obesity results in increased ROS production, which might lead to creation of senescent bone marrow microenvironment and stem cell exhaustion contributing to bone fragility in metabolic bone diseases Curr Osteoporos Rep (2019) 17:44 -454 6 447

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Effect of Glucagon-like Peptide-1 on the Differentiation of Adipose-derived Stem Cells into Osteoblasts and Adipocytes

Cited by 35 publications

References 40 publications

Cell Therapy Products in Alzheimer Disease

Cell Therapy Products in Alzheimer Disease

Effects of gastric inhibitory polypeptide, glucagon‐like peptide‐1 and glucagon‐like peptide‐1 receptor agonists on Bone Cell Metabolism

Insulin Signaling in Bone Marrow Adipocytes

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