Stem Cells as a Treatment for Chronic Liver Disease and Diabetes

Levičar, Nataša; Dimarakis, Ioannis; Flores, Catherine; Tracey, Jocelyn; Gordon, Myrtle Y.; Habib, Nagy

doi:10.1007/978-3-540-68976-8_11

Cited by 19 publications

(14 citation statements)

References 83 publications

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“…Approaches using cell differentiation of embryonic stem (ES) cells, somatic stem (SC) cells, or induced pluripotent stem (iPS) cells have recently received major attention for organ regeneration [16][17][18]; however, approaches using these cells have several problems including ethical issues and an insufficient supply. Use of stem cells also appears to allow regeneration of cells with relatively simple tissues such as blood vessels and muscle, but it remains unclear whether this approach can regenerate parenchymal or solid organs such as pancreas and liver, which have multiple functions.…”

Section: Pathophysiological Profiles Of Vmh-lesioned Micementioning

confidence: 99%

Cell proliferation in visceral organs induced by ventromedial hypothalamic (VMH) lesions: Development of electrical VMH lesions in mice and resulting pathophysiological profiles

et al. 2011

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AnimAl models of obesity are mainly categorized as hypothalamic, genetic and diet-induced obesity [1,2]. Hypothalamic obesity was first identified by Hetherington and Ranson [3] in 1940, based on the observation that obesity was produced by electrical destruction of bilateral ventromedial hypothalamic nuclei (VMH) in rats. Subsequently, hypothalamic obesity has been thought of exclusively as obesity induced by VMH lesions. However, it is now recognized that hypothalamic obesity is also produced by the destrucCell proliferation in visceral organs induced by ventromedial hypothalamic (VMH) lesions: Development of electrical VMH lesions in mice and resulting pathophysiological profiles Abstract. We have found that ventromedial hypothalamic (VMH) lesions produced by electrocoagulation induce cell proliferation in visceral organs through vagal hyperactivity, and also stimulate regeneration of partially resected liver in rats. To facilitate identification of proliferative and/or regenerative factors at the gene level, we developed electrical production of VMH lesions in mice, for which more genetic information is available compared to rats, and examined the pathophysiological profiles in these mice. Using ddy mice, we produced VMH lesions with reference to the previously reported method in rats. We then examined the pathophysiological profiles of the VMH-lesioned mice. Electrical VMH lesions in mice were produced using the following coordinates: 1.6 mm posterior to the bregma, anteriorly; 0.5 mm lateral to the midsagittal line, transversely; and 0.2 mm above the base of the skull, vertically, with 1 mA of current intensity and 10 s duration. The VMH-lesioned mice showed similar metabolic characteristics to those of VMH-lesioned rats, including body weight gain, increased food intake, increased percentage body fat, and elevated serum insulin and leptin. However, there were some differences in short period of hyperphagia, and in normal serum lipids compared to those of VMHlesioned rats. The mice showed a similar cell proliferation in visceral organs, including stomach, small intestine, liver, and, exocrine and endocrine pancreas. In conclusion, procedures for development of VMH lesions in mice by electrocoagulation were developed and the VMH-lesioned mice showed pathophysiological profiles similar to those of VMH-lesioned rats, particularly in cell proliferation in visceral organs. These findings have not been observed previously in gold thioglucoseinduced VMH-lesioned mice. This model may be a new tool for identifying factors involved in cell proliferation or regeneration in visceral organs. [5,6], and biochemical changes including hypergastric acid secretion [7,8], hyperlipidemia [1], hyperinsulinemia [1,9], and hyperleptinemia [10,11]. Furthermore, we found cell proliferation in visceral organs (liver, stomach, small intestine, and pancreas) in these rats using [3 H] thymidine uptake [12][13][14]. We also found that cell proliferation in vis-

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Section: Pathophysiological Profiles Of Vmh-lesioned Micementioning

confidence: 99%

Cell proliferation in visceral organs induced by ventromedial hypothalamic (VMH) lesions: Development of electrical VMH lesions in mice and resulting pathophysiological profiles

et al. 2011

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“…For example, recent published data has used human CD34+ adult bone marrow stem cells for the treatment of chronic liver disease and has shown an impressive outcome [Gordon et al, 2006;Levicar et al, 2008]. Haematopoietic stem cells have also being used in many clinical (Phase I) trails in the treatment of ischaemic heart disease, diabetes and other neurodegenerative diseases with an impressive preliminary outcome [Balsam and Robbins, 2005;Dimarakis et al, 2005;Levicar et al, 2007]. However, long-term outcome clinical data has still to be documented and carefully evaluated.…”

Section: Stem Cells and Clinical Relevance To Therapymentioning

confidence: 99%

Cancer Stem Cells and Chemoresistance

Chuthapisith¹

2011

Cancer Stem Cells Theories and Practice

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“…Expansion of embryonic stem (ES) cells, existing hepatocytes from the liver, and progenitor cells from bone marrow are techniques currently under investigation for regeneration of hepatocytes. However, therapeutic use of hepatocytes and ES cells is limited due to inadequate proliferation of mature hepatocytes, ethical and tumorigenic issues of ES cells and the requirement for immuno suppression [6] .…”

Section: Original Articlementioning

confidence: 99%