Unless noted otherwise, all medical/health advice has been given by non-medically qualified personnel.
All advice given on this site is designed to support and not replace any advice given by your personal physician.
If you have questions or concerns about individual health matters or the management of your diabetes, please consult your diabetes care team.
Seared tuna with butter beans and roasted tomatoes

Preheat the oven to 180ºC / 350ºF / gas mark 4. Mix together the cumin, coriander seeds and chilli flakes, press into both sides of the tuna and set aside for 30 minutes to allow the flavours to develop. Meanwhile, heat the oil in a small pan and fry the onion and garlic for 2-3 minutes. Transfer to an ovenproof dish with the butter beans and tomatoes, place in the oven for 30 minutes until the tomatoes begin to char. Heat a griddle pan until smoking and sear the tuna for about 1 m ...

See full recipe & ingredients

Site Update - Aug 2012
25 Jul 2012
Due to the upcoming re-launch and re-branding of the group, the site is being operated as a separate ... Read more
South Sefton Diabetes Group Update - Aug 2012
25 Jul 2012
Due to a decrease in attendance at the group meetings, the Chairman has requested a re-launch from D ... Read more
Recipe of the day
25 Jul 2012
Each day, a new recipe from our database will be selected for display on the index page. It will sh ... Read more
For more news posts, please visit our news section related article links
Show Hide
Type 1 diabetes research breakthrough as Australian researchers challenge T cell immunology
A breakthrough by Australian researchers could change the way T cell receptors (TCRs) are studied, and have implications for type 1 diabetes. A team at Monash University have demonstrated for the first time that TCRs can bind to immune molecules known as the major histocompatibility complex (MHC) in a completely reversed orientation. When TCRs bind to MHC, this signals that a T cell is infected and T cells launch an attack of the area reported as being infected. This finding contradicts the current assumption held by scientists that TCRs must bind to MHC in a specific orientation to create a signal to the immune system. Type 1 diabetes and T cells Earlier this year, British scientists identified a particular type of T cell - the follicular helper T cell - that triggers an immune response which leads to type 1 diabetes. This T cell results in the destruction of insulin-producing cells, and the body cannot produce insulin, which is responsible for regulating blood glucose levels. This new discovery about the way immune cells work could result in forthcoming studies aimed at identifying how the immune system attacks insulin-producing beta cells, which characterises type 1 diabetes. Monash researchers had been investigating TCRs associated with a regulatory T cell (Treg), which prevents the body from attacking its own insulin-producing cells. Co-author Dr. Hugh Reid, Monash University, explained: "In type 1 diabetes there are not enough of these peacekeeping {Treg} cells and so the immune system continues to attack and destroy insulin-secreting cells." Immunologists have long believed that TCRs only function when they interact with MHC in a "fixed" way, and that for T cells to be activated, they must "dock" in this fashion. Using a fragment of insulin protein and an MHC molecule, production of Treg cells was stimulated, and despite a reversed mode of connection, the cells still suppressed the attacking immune response in the presence of insulin. By suggesting that all types of T cells could connect with MHC in a different order, the researchers have challenged established views and opened up further research opportunities. "We will now set out to determine more TCR-MHC interactions of the same regulatory T cell subset and compare them to the other T cell TCR-MHC interactions derived from the inflammatory T cells," added Reid.
Low cognitive function associated with impaired fasting glucose in late adolescence, study finds
Low cognitive function is linked to impaired fasting glucose in late adolescence, according to new research. The study, conducted by researchers at Chaim Sheba Medical Centre in Israel, found that the general intelligence score (GIS) of each participant affected their risk of impaired fasting glucose. Based on their GIS, 17,348 adults without diabetes or impaired fasting glucose were divided into three groups: low score, medium score and high score. 87 per cent of participants were men, with a mean age of 31 years. The GIS scores were taken from the participants at the age of 17. The researchers measured the fasting plasma glucose levels of the participants every three to five years. The researchers found that the participants in the lowest GIS group of had a significantly higher risk of impaired fasting glucose than participants in the highest group. "On a clinical level, along with family history of diabetes, fasting plasma glucose, [triglyceride] level, [white blood cell] counts and BMI, assessment of cognitive function may serve as a marker of overall health and aid in the identification of those at increased risk of dysglycemia," the researchers wrote. "On a research level, these findings may be the basis for further research exploring the mechanistic routes that underlie the cognitive-dysglycemia relationship." The findings were published in the Journal of Clinical Endocrinolgy and Metabolism.
Metformin tolerance influenced by genetic variants and other medication, study finds
Certain genetic variants may interfere with gut absorption of metformin, leading to severe intolerance, according to new research. The study, presented at the European Association for the Study of Diabetes (EASD) 2015 Meeting, suggested that the 20 per cent of people who experience side effects after taking metformin could be victims of these genetic variants. The particular genetic variant in question is organic cation transportion 1 (OCT1), a protein involved in the absorption and elimination of metformin. The researchers identified several medications that prevent OCT1 from transporting metformin, including certain antidepressants and proton-pump inhibitors. "The pathophysiology isn't known but is hypothesised to be related to a high concentration of metformin in the intestine following oral administration," explained Tanja Dujic, who was a researcher at the University of Sarajevo when the study was conducted. Previous research found that around eight per cent of the population has inactive OCT1 alleles, which seriously impaired their metformin tolerance. The participants were then given medication to inhibit OCT1, which exacerbated their metformin intolerance even further. This study involved 2166 participants, all of whom had recently begun to take metformin to treat type 2 diabetes. 251 of the participants were considered intolerant, and the intolerant patients were around 10 years older, more likely to be female, tended to have a lower body mass index (BMI), and had a lower HbA1c on average. 48 per cent of the participants who were metformin intolerant took OCT1-inhibiting drugs. Only 33 per cent of metformin-tolerant participants took OCT1-inhibiting drugs. The OCT-1 inhibiting drugs most strongly associated with metformin intolerance were verapamil, codeine, citalopram, doxasozin, and PPIs. If you take any of these medications along with metformin, and you are concerned about the effects, speak to your doctor before making any changes to your medication. The findings were published in the journal Diabetes.
More than 60 per cent of patients with type 2 diabetes have fatty liver disease, study finds
More than 60 per cent of patients with type 2 diabetes show signs of non-alcoholic fatty-liver disease (NAFLD), according to new research. The study, conducted by researchers at the University of California, San Diego, also established a link between NAFLD and many aspects of metabolic syndrome, including hypertension and larger waist. The researchers analysed the data of 100 adult patients, all of whom had type 2 diabetes. On average, the participants had a BMI of 30.8, and had had type 2 diabetes for 8.5 years. Each participant was scanned to assess the presence of NAFLD. 65 per cent of participants showed signs of NAFLD. Surprisingly, the prevalence of NAFLD was lower in older participants, and higher in younger ones. Almost 79 per cent of participants under the age of 58 had NAFLD, compared to 68 per cent of participants between the ages of 58 and 65, and 47 per cent of those over 65. The researchers concluded that current methods of screening for NAFLD are inaccurate. Certain predictors of NAFLD progression may help clinicians to make an early diagnosis, including lower levels of "good" HDL cholesterol, higher triglyceride levels and greater mean waist circumference. "Most patients have no idea that they have fatty-liver disease until they develop cirrhosis, and that's why it's a silent killer," said senior author Rohit Loomba, MD, Associate Professor of Clinical Medicine at the University of California, San Diego, to Medscape Medical News. "But the beautiful thing about the liver is that it can regenerate, and many new therapies are in the pipeline for the treatment for NAFLD and NAFLD-related fibrosis. "So identification of these patients is key: we will be able to be able to stop progression of disease; we will be able to reverse cirrhosis and fibrosis with these new therapies, and we already are doing so in some patients. "If physicians have a patient with three or four features of the metabolic syndrome and they are diabetic, I can almost guarantee you that they have if physicians have patients like this, they need be to asking themselves: 'Am I missing liver disease here?' and refer them to a hepatologist for evaluation." The findings were published in Alimentary Pharmacology and Therapeutics.
More exercise required for people at risk of type 2 diabetes, study reports
People with an increased risk of type 2 diabetes need to exercise more to achieve similar results to those without type 2, according to new research. Scientists from Lund University, Sweden investigated the effects of exercise on people whose increased risk of type 2 was caused by having an immediate relation to someone with the disease. 50 unfit men in their 40s who were slightly overweight, but otherwise completely healthy were recruited for the trial. Half of them had relatives with type 2 diabetes, while the other 25 served as controls. The participants exercised regularly at a fitness session, which involved three training sessions a week: two aerobic classes and one spinning class. Exercise intensity and energy consumption were measured by researchers. The at-risk group attended more sessions and also expended more energy than the control group. Both groups lost weight and reduced their waist size, but the results were similar between the groups. Lead author Ola Hansson said: "The difference was that participants from the risk group had to exercise more to achieve the same results as the participants from the control group. "It is interesting to see that there is a difference despite the fact that all of them are actually healthy and otherwise very similar. We now hope to continue with further studies, including examining whether exercise intensity rather than volume is a crucial factor in determining how the risk group responds to exercise." Lund University researchers are now planning to investigate if a particular type of exercise is more effective in preventing type 2 diabetes among at-risk groups.
Second trial for insulin vaccination against type 1 diabetes
An insulin vaccination trial will test whether giving very young children oral insulin can prevent type 1 diabetes in the long-term. German children between the ages of six months and two years who have a first-degree relative with type 1 diabetes will be recruited for the Pre-POINTearly vaccination study. This trial follows up on the Pre-POINT study, an international collaboration coordinated by Professor Dr. Ezio Bonifacio at the Centre for Regenerative Therapies Dresden (CRTD), Germany. The first study observed a positive immune response in children at risk of type 1 diabetes who were administered oral doses of insulin. The insulin was well tolerated by the children and shown to be safe. The Pre-POINTearly vaccination study will treat children with powdered insulin who have not developed an autoimmune response. Their daily dose will increase gradually from 7.5mg to 6.75mg and medical examinations will be conducted at three-month intervals. The researchers hope the oral insulin - which does not affect blood glucose levels as it is absorbed in the mouth and intestines before splitting into smaller components during digestion - could prevent the autoimmune destruction of insulin-producing beta cells and stimulate the growth of protective immune cells. Prof. Anette-Gabriele Ziegler, Director of the Institute of Diabetes Research said: "The autoimmune response that causes type 1 diabetes in childhood is often initially directed at the insulin. The aim of the Pre-POINTearly study is therefore to build up immune tolerance to insulin and thus block the autoimmune process."
One third of diabetes patients do not report nocturnal hypoglycemia to doctor
A survey from Novo Nordisk finds that 50 per cent of people with diabetes suffer night-time hypoglycemia, while one third of people did not report this to their doctor. The results from this survey coincide with Hypo Awareness Week (October 5-11), which annually stresses greater awareness of hypo symptoms among healthcare professionals, and communication between patients and doctors. Novo Nordisk, the official partner for Hypo Awareness Week, have launched the awareness campaign TALK Hypos alongside the survey. The campaign, supported by Diabetes UK, encourages people who experience hypoglycemia to talk about this with their doctor or nurse. Novo Nordisk has recently released their long-acting insulin Tresiba (insulin degludec), that has been shown to reduce instances of nocturnal hypoglycemia. Nocturnal hypoglycemia 500 people with type 1 and type 2 diabetes were surveyed by Novo Nordisk - two thirds of whom had experienced a night-time hypo in the month prior to the survey. Night-time hypos led to a significant impact on people's lives. 21 per cent reported missing work, while 12 per cent suffered a loss of productivity at work. 13 per cent experienced a reduced desire to socialise, and a 12 per cent lost incentive to exercise. More alarmingly, 14 per cent reported that they had physically injured themselves during a night-time hypo, and 25 per cent are scared to be alone when suffering nocturnal hypoglycemia. Concerns have also been raised that one third of participants did not report night-time hypos to their doctor or nurse, despite the problems that it caused them. Professor Anthony Barnett, Emeritus Professor of Medicine, University of Birmingham, said: "It is concerning that some patients are not reporting night-time hypos to their doctor or nurse, given the impact on their long-term health and lifestyle. "People with diabetes who are experiencing either day- or night-time hypos are encouraged to speak to their doctor or nurse to ensure that they are being appropriately managed." If you are struggling with night-time hypos, or your hypo awareness in general, then you can improve your diabetes control with the Hypo Awareness Program, a completely free education course. 75 per cent report that their understanding of hypo awareness improved following the course, which focuses on enhancing your knowledge of hypo symptoms. The Hypo Awareness Program takes 30 seconds to sign up and can be completed at your own pace. It can also result in fewer cases of severe hypoglycemia among people with diabetes.
Novel technique reboots insulin production in pancreatic cells
A technique to "reboot" pancreatic cells so insulin can be secreted has been developed by Belgian researchers. The Université Catholique de Louvain believes this finding could be further developed so people with type 1 diabetes can control blood glucose levels without requiring daily injections. A team led by Phillipe Lysy investigated human pancreatic duct-derived cells (HDDCs) that were taken from non-diabetic donors after their deaths. The HDDCs - which don't produce insulin, but can grow into different types of cells - were reprogrammed to act like insulin-producing beta cells by being exposed to fatty particles. To achieve this, the researchers used messenger RNA (mRNA) of a transcription factor, which carries DNA code to other parts of the cell for processing. Using mRNA, the fatty particles carried the genetic code to make MAFA, which allows genes to be switched on or off in the genome. The mRNA was then transformed into protein before binding to DNA in the nucleus and activating insulin production. When these altered cells were implanted into diabetic mice models, the researchers checked that insulin was being secreted. According to Lysy, "the results are encouraging". "With ongoing in vivo studies, we are analyzing the potential of our reprogrammed cells to function and secrete insulin into a body according to blood glucose levels. Our objectives are to evaluate the conditions that allow banking of our reprogrammed cells in clinically compatible procedures," Lysy said. Lysy and his team added that a further benefit of this novel treatment is that it offsets the risks related to stem cell treatments, such as cancer and structural modifications to DNA. The technique could be ready for human testing in three to five years if work continues to progress. The researchers hope that cells could be harvested from the HDDCs of dead donors and converted into a mass of insulin-producing cells. The findings were reported at the 54th Annual European Society for Paediatric Endocrinology Meeting in Barcelona, Spain.
Technological advances have increased the life expectancy of people with type 1 diabetes, study finds
The life expectancy of people with type 1 diabetes has improved significantly in recent years, thanks to technological advances allowing for careful management of blood glucose levels. The findings come from a study conducted by a team of endocrinologists at the Royal Melbourne Hospital. There are twice as many cases of type 1 diabetes as there were 20 years ago, an increase that has led to a number of technological advances in its treatment: more accurate blood glucose meters, insulin pumps, smartphone apps and continuous glucose monitors (CGMs) have all contributed to a longer life expectancy for people with type 1 diabetes. However, type 1 diabetes is still associated with a shorter life expectancy than people without diabetes. "Despite recent advances, T1D is still associated with considerable premature mortality caused by acute and chronic complications, particularly ischaemic heart disease," wrote the researchers. "The presence and severity of chronic kidney disease and ischaemic heart disease predict all-cause mortality in T1D. Recent reports of improved life expectancy...provide great hope for persons with T1D and their clinicians." Nevertheless, "recent findings show that a significant improvement in life expectancy has occurred," wrote the researchers. Along with better management, recent advances have led researchers to be hopeful that a cure will be available in the reasonably near future. Several studies have managed to prevent type 1 diabetes at various stages. "The ability to predict T1D on the basis of genetic, immunological and metabolic markers has provided opportunities for prevention at different preclinical stages," the researchers wrote. "Much attention has focused on interventions at diagnosis and in the preclinical antibody positive stage." One of the most promising methods of treating type 1 diabetes remains islet cell transplantation. However, it isn't currently viable on a widespread basis. It often requires the cells of several donors to treat one patient, and donors are few as it is. Even when the transplant has been carried out successfully, the recipient has to take immunosuppressant drugs for the foreseeable future to prevent the immune system from rejecting the new cells, leaving them at risk of a number of other diseases. "Limited tissue supply is a key barrier to more widespread use of islet transplantation. Advances in stem-cell technologies or in the production of porcine islets for human transplant may overcome this problem in the future." The findings were published in the Medical Journal of Australia.
Fructose breakthrough could lead to future diabetes and obesity treatments
A breakthrough in understanding how fructose is transported into our cells could lead to the development of novel treatments for diabetes, cancer and obesity. An international collaboration between researchers from Stockholm University, the UK and Japan investigated how fructose, also known as fruit sugar, is absorbed into cells from the blood. Fructose is one of the main sugars in our diet and is found in vegetables, honey and fruits. When consumed this way, fructose is harmless due to the additional vitamins in these foods, but fructose affects the brain in a different way when added to products such as ready meals and sugary drinks. Using a technique called x-ray crystallography, researchers identified how the protein GLUT5 transports fructose through the cell membrane. When activity of GLUT5 is altered, it has been linked to type 2 diabetes and obesity, the researchers report. Following analysis of how the atoms in GLUT5 are positioned, the researchers built three-dimensional models of GLUT5 which could mark an important step in research on diseases such as diabetes and cancer, which are related to sugar uptake. Lead researcher Dr. David Drew, Department of Biochemistry and Biophysics at Stockholm University, said: "By revealing how the fructose transporter functions at the atomic level, we can now begin to understand other things about it. For example, how this gate-keeper is selective to fructose from all other thousands of other molecules our cells are constantly bombarded by." The study was published in the journal Nature.