Stem Cell Treatment Diabetes

Stem Cell Treatment for Diabetes is an Option

STEM CELL TREATMENT DIABETESDiabetes mellitus, often simply referred to as diabetes, is a group of metabolic diseases in which a person has high blood sugar, either because the body does not produce enough insulin, or because cells do not respond to the insulin that is produced. This high blood sugar produces the classical symptoms of polyuria (frequent urination), polydipsia (increased thirst) and polyphagia (increased hunger).

There are three main types of diabetes:

  • Type 1 diabetes: results from the body's failure to produce insulin, and presently requires the person to inject insulin. (Also referred to as insulin-dependent diabetes mellitus, IDDM for short, and juvenile diabetes.)
  • Type 2 diabetes: results from insulin resistance, a condition in which cells fail to use insulin properly, sometimes combined with an absolute insulin deficiency. (Formerly referred to as non-insulin-dependent diabetes mellitus, NIDDM for short, and adult-onset diabetes.)
  • Gestational diabetes: is when pregnant women, who have never had diabetes before, have a high blood glucose level during pregnancy. It may precede development of type 2 DM.

Stem Cell Treatment and Diabetes

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Related Articles Protein Phosphatase PP5 Controls Bone Mass and the Negative Effects of Rosiglitazone on Bone through Reciprocal Regulation of PPARγ (Peroxisome Proliferator-activated Receptor γ) and RUNX2 (Runt-related Transcription Factor 2). J Biol Chem. 2016 Nov 18;291(47):24475-24486 Authors: Stechschulte LA, Ge C, Hinds TD, Sanchez ER, Franceschi RT, Lecka-Czernik B Abstract Peroxisome proliferator-activated receptor γ (PPARγ) and runt-related transcription factor 2 (RUNX2) are key regulators of mesenchymal stem cell (MSC) differentiation toward adipocytes and osteoblasts, respectively. Post-translational modifications of these factors determine their activities. Dephosphorylation of PPARγ at Ser-112 is required for its adipocytic activity, whereas phosphorylation of RUNX2 at serine 319 (Ser-319) promotes its osteoblastic activity. Here we show that protein phosphatase 5 (PP5) reciprocally regulates each receptor by targeting each serine. Mice deficient in PP5 phosphatase have increased osteoblast numbers and high bone formation, which results in high bone mass in the appendicular and axial skeleton. This is associated with a substantial decrease in lipid-containing marrow adipocytes. Indeed, in the absence of PP5 the MSC lineage allocation is skewed toward osteoblasts and away from lipid accumulating adipocytes, although an increase in beige adipocyte gene expression is observed. In the presence of rosiglitazone, PP5 translocates to the nucleus, binds to PPARγ and RUNX2, and dephosphorylates both factors, resulting in activation of PPARγ adipocytic and suppression of RUNX2 osteoblastic activities. Moreover, shRNA knockdown of PP5 results in cells refractory to rosiglitazone treatment. Lastly, mice deficient in PP5 are resistant to the negative effects of rosiglitazone on bone, which in wild type animals causes a 50% decrease in trabecular bone mass. In conclusion, PP5 is a unique phosphatase reciprocally regulating PPARγ and RUNX2 activities in marrow MSC. PMID: 27687725 [PubMed - indexed for MEDLINE]
Related Articles Stem cells to restore insulin production and cure diabetes. Nutr Metab Cardiovasc Dis. 2017 Feb 21;: Authors: Sordi V, Pellegrini S, Krampera M, Marchetti P, Pessina A, Ciardelli G, Fadini G, Pintus C, Pantè G, Piemonti L Abstract BACKGROUND: The advancement of knowledge in the field of regenerative medicine is increasing the therapeutic expectations of patients and clinicians on cell therapy approaches. Within these, stem cell therapies are often evoked as a possible therapeutic option for diabetes, already ongoing or possible in the near future. AIM: The purpose of this document is to make a point of the situation on existing knowledge and therapies with stem cells to treat patients with diabetes by focusing on some of the aspects that most frequently raise curiosity and discussion in clinical practice and in the interaction with the patient. In fact, at present there are no clinically approved treatments based on the use of stem cells for the treatment of diabetes, but several therapeutic approaches have already been evaluated or are being evaluated in clinical trials. DATA SYNTHESIS: It is possible to identify three large potential application fields: 1) the reconstruction of the β cell mass; 2) the immunomodulation in type 1 diabetes (T1D); 3) the treatment of complications. In this study we will limit the discussion to approaches that have the potential for clinical translation, deliberately omitting aspects of basic biology and preclinical data. Also, we intentionally omit the treatment of the complications that will be the subject of a future document. Finally, an overview of the Italian situation regarding the storage of cord blood cells for the therapy of diabetes will be given. PMID: 28545927 [PubMed - as supplied by publisher]
Related Articles Green tea EGCG enhances cardiac function restoration through expression of survival signaling in DM rats with autologous adipose tissue-derived stem cell. J Appl Physiol (1985). 2017 May 25;:jap.00471.2016 Authors: Chen TS, Liou SY, Kuo CH, Pan LF, Yeh YL, Liou J, Padma VV, Yao CH, Kuo WW, Huang CY Abstract The present study tests a hypothesis that cardioprotective effects mediated by autologous adipose-derived stem cells (ADSC) in rats afflicted with insulin-dependent diabetes mellitus (IDDM), may be synergistically enhanced by oral treatment with green tea epigallocatechin gallat (ECCG). Wistar rats were divided into sham, DM, DM+ADSC (autologous transplanted 1x106 cells/rat) and DM+ADSC+E (E, green tea oral administration EGCG). Heart tissues were isolated for all rats and investigations were performed after 2-months treatment. In the groups of sham, DM and DM+ADSC, we can find that DM induces cardiac-dysfunction (sham and DM) and autologous transplantation of ADSC can partially recover cardiac functions (DM and DM+ADSC) in DM rats. Compared to DM+ADSC, significant improvement in cardiac-functions can be observed in DM+ADSC+E in echocardiographic data, histological observations and even in cellular protein expression. Oral administration of green tea EGCG and autologous transplantation of ADSC show synergistically beneficial effects on diabetic cardiacmyopathy in DM rats. PMID: 28546469 [PubMed - as supplied by publisher]
Metformin increases chemo-sensitivity via gene downregulation encoding DNA replication proteins in 5-Fu resistant colorectal cancer cells. Oncotarget. 2017 May 11;: Authors: Kim SH, Kim SC, Ku JL Abstract Metformin is most widely prescribed for type 2 diabetes. Recently, evidences have shown that metformin has anticancer effects on pancreatic-, colorectal-, ovarian-, and other cancers. Because metformin has less adverse effects and is inexpensive, it could be a useful chemo-therapeutic agent with anticancer effects. In this study, we demonstrated metformin inhibited by cell proliferation, cell migration ability, clonogenic ability, and cancer stem cell population. Metformin also induced cell cycle arrest in parental-(SNU-C5), and 5-Fu resistant-colorectal cancer cell line (SNU-C5_5FuR). Moreover, a treatment that combines 5-Fu and metformin was found to have a synergistic effect on the cell proliferation rate, especially in SNU-C5_5FuR, which was mediated by the activation of AMPK pathway and NF-ƙB pathway, well-known metformin mechanisms. In this study, we suggested novel anticancer mechanism of metformin that inhibited DNA replication machinery, such as the MCM family in SNU-C5_5FuR. In conclusion, we provided that how metformin acts as not only a chemo-sensitizer, but also as a synergistic effector of 5-Fu in the 5-Fu resistant-cell line. We speculate that metformin used for adjuvant therapy is effective on 5-Fu resistant cancer cells. PMID: 28549344 [PubMed - as supplied by publisher]

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