Making beta cells from people with type 1 diabetes Research Update Dec. 27, 2016 Scientists generated functional β (beta) cells from the skin cells of people with type 1 diabetes. In type 1 diabetes, a misguided attack by the immune system leads to destruction of insulin-producing β cells found in clusters called islets in the pancreas. Although administration of insulin via injections or a pump is life-saving, it does not mimic the exquisite blood glucose (sugar) control of the pancreas. Therefore, scientists are pursuing strategies to replace the destroyed β cells. One way to do that is through islet transplantation-an experimental procedure using islets from a cadaveric donor. The procedure has shown promise for people with difficult-to-control diabetes, but has significant challenges: donor islet tissue is limited, and immunosuppressive medications, which have toxic side effects, are required to prevent rejection of tissue transplanted from another individual. Toward overcoming the first barrier, scientists recently developed a new laboratory production method to make large quantities of β cells-called stem-cell derived β (SC-β) cells-from human stem cells. This method could, with further development, be used to make β cells from a sample of cells from a person with type 1 diabetes in the quantities needed for transplantation back into that same person. These cells would likely require protection from the autoimmune attack, but might not require toxic immunosuppressive medications to prevent rejection of the tissue. To investigate this possibility, in new research, scientists used skin cells from three people with type 1 diabetes (T1D cells) and three people without diabetes (ND cells). By introducing specific factors into these cells and using the new large-scale production method they developed, they made the skin cells become stem cells-cells that could subsequently become any cell type. They then, by introducing other factors, coaxed these stem cells to become SC-β cells (T1D SC-β cells and ND SC-β cells). Cells from the two different origins showed no differences in the ability to become SC-β cells, indicating for the first time that cells from a person with type 1 diabetes could be used to make SC-β cells. Next, the scientists demonstrated that the T1D SC-β cells functioned like healthy β cells. For example, in laboratory culture, T1D SC-β cells secreted insulin in response to glucose; they also released insulin in response to diabetes drugs that are known to stimulate insulin secretion, demonstrating their potential for use in screening for new diabetes drugs. The T1D SC-β also functioned in live animals: when T1D SC-β cells were transplanted into male mice, they produced insulin in response to glucose and controlled the animals’ blood glucose levels. Many research questions remain before an SC-β cell transplant procedure will be ready for testing in humans. First, it remains possible that differences between T1D

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Gastric band Surgery In France Being overweight may be more harmful than you thought Sign in Log in with your Medical News Today account to create or edit your custom homepage, catch-up on your opinions notifications and set your newsletter preferences. Sign in Register for a free account For FREE No Obligation Information about the cost of Gastric Band Surgery in France Click here Or Click the Image Below to visit our Special offer Page to see if you Qualify for any Discounts Read more……>click Here< Read more... Read more…

Genome-Wide Association Study of Primary Sclerosing Cholangitis Identifies New Risk Primary sclerosing cholangitis (PSC) is a rare progressive disorder leading to bile duct destruction; ∼75% of patients have comorbid inflammatory bowel disease (IBD). We undertook the largest genome-wide association study of PSC (4,796 cases and 19,955 population controls) and identified four new genome-wide significant loci. The most associated SNP at one locus affects splicing and expression of UBASH3A, with the protective allele (C) predicted to cause nonstop-mediated mRNA decay and lower expression of UBASH3A. Further analyses based on common variants suggested that the genome-wide genetic correlation (rG) between PSC and ulcerative colitis (UC) (rG = 0.29) was significantly greater than that between PSC and Crohn’s disease (CD) (rG = 0.04) (P = 2.55 × 10-15). UC and CD were genetically more similar to each other (rG = 0.56) than either was to PSC (P < 1.0 × 10-15). Our study represents a substantial advance in understanding of the genetics of PSC. Read more......>click Here< Read more... Read more…

Figure 1 Functional characterization of Atxn1, Ebf1, Rreb1 and Ube2e2 (a,b,e) Data is displayed as box/whisker plots where the center line represents the median, box limits contain the 25th-75th percentiles, and whiskers span max/min values.(a) Gene expression measured by qPCR in murine subcutaneous (SAT), perigonadal visceral (VAT), and pericardial (PAT) adipose tissues (n=6 mice). Statistical significance was assessed using ANOVA and Sidak’s correction for multiple comparisons.(b) Gene expression measured by qPCR in murine adipose tissues after 8 weeks of high fat feeding compared to normal chow fed controls (n=5 mice per group). Statistical significance was assigned using a two-sided T-test.(c) Gene expression measured by qPCR in cultured adipocyte progenitors isolated from the subcutaneous (SAT) or perigonadal visceral (VAT) depots (n=4 replicates). Cells were expanded to confluence and then collected at intervals after induction of adipogenic differentiation. Data displayed as mean, error bar=s.e.m. Statistical significance was assessed using ANOVA and Sidak’s correction for multiple comparisons to time 0.(d) Oil-red-o staining of progenitors isolated from subcutaneous adipose and exposed to retroviral delivery of shRNA constructs during ex vivo expansion and induction of adipogenesis. Relative to control vector carrying a scramble sequence, shRNA constructs specific for Atxn1 and Ube2e2 impaired adipogenic differentiation. Scale=1mm.(e) Oil-red-o stain was alcohol extracted and quantified at OD520 (n=9 technical replicates). Statistical significance was assessed using ANOVA and Sidak’s correction for multiple comparisons to control (Scramble). Data representative of 3 independent experiments. Read more……>click Here< Read more... Read more…

Gastric band Surgery In France Does living next to a gym lower obesity risk? Sign in Log in with your Medical News Today account to create or edit your custom homepage, catch-up on your opinions notifications and set your newsletter preferences. Sign in Register for a free account For FREE No Obligation Information about the cost of Gastric Band Surgery in France Click here Or Click the Image Below to visit our Special offer Page to see if you Qualify for any Discounts Read more……>click Here< Read more... Read more…

Gastric band Surgery In France Could this device help to prevent the harms of sitting? Sign in Log in with your Medical News Today account to create or edit your custom homepage, catch-up on your opinions notifications and set your newsletter preferences. Sign in Register for a free account For FREE No Obligation Information about the cost of Gastric Band Surgery in France Click here Or Click the Image Below to visit our Special offer Page to see if you Qualify for any Discounts Read more……>click Here< Read more... Read more…

Compare Affordable Bariatric Surgery in France cost of gastric band surgery Type 2 Diabetes and Weight Loss – Tips to Help You Eat Smart When Dining Out Whether you are on a diet or not, you are going to dine out now and then. Ideally, it will not be too often, because it is better for your health to be cooking the majority of your meals yourself. But considering you will have social events and you will want to eat out on occasion, it is important to know how to do it correctly. Even if you are following a weight loss protocol, it is possible to eat out and not hinder your progress. If you have Type 2 diabetes, you can still eat out without having to ask for a diabetic-friendly meal. But there are some things you must do… 1. Getting up off the couch and taking part in regular physical activity is one of the most important things you can do to ensure you remain healthy. < !13926-20180112013430!> 2. Read the nutrition information. To build on the previous point, you should read the nutrition information for the meals that grab your attention. Nowadays, you are more likely to be able to do this than ever before. Either look up the information on the website or ask for the nutrition menu. Sometimes you will find a breakdown on the main menu itself. 3. Order your meal first. The influence of your peers is not always helpful: this is particularly the case at a restaurant. You will be more likely to stick to your first, healthy choice by ordering first. Otherwise, you might second guess yourself and be more liable to go for your second option. 4. Don’t get distracted. Distraction is the primary reason we overeat in social settings. We get carried away in conversation and forget to pay attention to our food. Sometimes, we do not even fully appreciate our meal, much less recognize how much we are consuming. Take care not to overeat. 5. Be careful with sides. Many times, side options are the main culprit. It is not the chicken bolognese that is the issue – it is the fries. Anything cooked in oil should be avoided most of the time.: this is particularly the case on a diet. Ask for a salad or mixed vegetables as your side when possible. 6. Be wary of appetizers. Appetizers taste great. But the benefits stop there. They are almost always packed with calories. Skip them, and look forward to your meal instead. 7. Drink water. Do not drink soda and do your best to avoid alcohol. They are empty calories. Ask for water – there is no better option. If you do drink alcohol, however, limit yourself to one drink. 8. Give yourself a break. Lastly, the final tip is to give yourself a break. While this runs contrary to everything else on the list, you have to remember you should not be hard on yourself all the time. If you have had a particularly good week when it comes to your diet, give yourself a much-deserved break. Eat what you would like most, as long as you do not go beyond your limits. Although managing your disease can be very challenging, Type 2 diabetes

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Compare Lowest Price Adjustable Gastric band Surgery overseas price of gastric band Weight loss surgery reduces cancer risk by 33 percent in womenA large retrospective study that focused mainly on women finds that cancer risk is reduced by almost a third after bariatric, or weight loss, surgery.See all stories on this topic Read more… Read more…

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Gastric band Surgery In France Diabetes: New pathway to treatment suggested by protein culprit What is the link between anxiety and diabetes? New research shows that a protein related to the development of anxiety and depression may also play a role in triggering diabetes. Scientists from the Max Planck Institutes hypothesize that an antagonist compound could be used to block its effect. Scientists investigate a new lead in the search for better diabetes treatments. The main known causes for type 2 diabetes so far include obesity and lack of physical exercise – both of which can lead to insulin resistance – as well as a family history of the condition. Insulin resistance occurs when muscles, liver, and fat cells become unable to use insulin appropriately, which ultimately leads to a dangerous rise in blood glucose levels. Now, researchers from the Max Planck Institute of Psychiatry in Munich, Germany, have found that a protein called FKBP51 may also play a role in triggering type 2 diabetes. The protein has so far been associated with anxiety and depression; it contributes to the regulation of the stress system. When the gene that controls the production of FKBP51 suffers a mutation, this can lead to dysregulation of the stress system, which, in turn, can cause mental health disorders. Mathias Schmidt – lead researcher of the current study – and colleagues have recently noted that the FKBP51 protein also contributes to forming a molecular link between the stress system and the regulation of various metabolic functions. This may make FKBP51 responsible for the onset of metabolic diseases such as obesity and diabetes. The team’s findings have now been published in the journal Nature Communications. Protein reacts to metabolic stress Schmidt and team looked at a mouse model to understand the potential role played by FKBP51 in metabolic processes. They studied the effect of a high-fat diet on mice in which the FKBP51 gene was expressed, as well as on knockout mice, in which that gene was inactivated artificially. They found that the knockout mice did not gain weight after exposure to the diet, had better glucose, or blood sugar, tolerance, and had more effective insulin signaling. This allowed the researchers to understand that the FKBP51 protein – regulated by the gene with the same name – affects signaling pathways in skeletal muscles. Since the protein is sensitive to metabolic stress factors, such as high fat intake, it can ultimately lead to blood sugar buildup and insulin resistance. These are the main factors to blame in the development of type 2 diabetes and obesity. “FKBP51 influences a signaling cascade in muscle tissue, which with excessive calorie intake leads to the development of glucose intolerance, i.e., the key indicator of diabetes type 2.” Mathias Schmidt The cause may lead to the treatment Fortunately, this mechanism has also offered the scientists an insight into how they might be able to prevent FKBP51’s response to the

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Gastric band Surgery In France How can we switch off hunger in the brain? Study sheds light Many of us think that controlling our food cravings and sticking to a diet depend largely on our willpower, but our biology has a different story to tell. Now, new research shows that a complex interplay between calories, digestion hormones, and neurons determines what we eat and when. What happens in our brain when we’re hungry, and is there anything we can do to shut down the feeling? While there may be some eating habits that we can control, our biology determines much of our appetite, and there’s more and more research that confirms this. For instance, at Medical News Today, we have recently reported on a study that identified a class of glial brain cells in our hypothalamus – that is, the appetite-controlling area of our brain – which, when activated by certain nutrients, “tell us” to stop eating. Another recent study found that a hormone called asprosin “turns on” our appetite-stimulating neurons and “turns off” our appetite-suppressing neurons. Now, researchers at the University of Pennsylvania in Philadelphia – led by J. Nicholas Betley, an assistant professor in the Department of Biology in the university’s School of Arts and Sciences – delve deeper into the interplay between our gut and our brain. The researchers looked at what it is that triggers our appetite-stimulating neurons, and – more importantly for our weight management efforts – what it is that switches them off. The findings, which were published in the journal Cell Reports, may change how we think about overeating and obesity and may soon lead to wholly new therapies and weight loss strategies. What are AgRP neurons? The so-called agouti-related protein-expressing neurons (AgRP) are neurons in our hypothalamus that become activated when we are hungry. As Betley explains, “When these neurons are firing, they’re basically telling you, ‘You’d better go get food; you’re starving.'” AgRP neurons are “a sensitive alarm system,” Betley says. But, apart from by eating, is there any other way that you can turn the alarm system off? Previous research led by Betley revealed that AgRP neurons deactivate when rodents eat, but interestingly, also when they see or smell the food. In other words, if you’re at a restaurant, feeling hungry, and waiting impatiently for your food – your AgRP neurons would be firing up in an impatient “chatter,” telling you to eat. But, as soon as the waiter brings the food to you and you can see and smell it, these neurons quickly pipe down. For the new study, however, the team wanted to look more closely at the difference between how these neurons are shut down upon eating, and how they are shut down by the mere sight and smell of incoming food. Nutrients switch off AgRP neurons To do so, Betley and team used in vivo calcium imaging – a method that allows the researchers to track the activity of neurons with a high degree of specificity – to study genetically

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