Diabetes management (London, England)最新文献

Aim: This study aimed to prospectively investigate transition beliefs, knowledge and needs of pediatric patients with diabetes and their parents.

Patients & methods: Parallel youth and parent questionnaires evaluating the transition process were distributed over a 6-month time period. Respondents included 123 pediatric patients with diabetes (11-19 years old) and their parents.

Results: Few families had discussed the transition of diabetes care (∼25%). Most had not established a transition plan (∼90%). Youth and parents agreed that seeing the doctor alone, discussions about transition and transition itself should occur at 17-18 years of age.

Conclusion: Youth with diabetes and their parents are not prepared for transition to adult care. Transition discussions should begin at an earlier age. Additional research is needed to learn how and when to begin these discussions.

Type 1 diabetes (T1D) results from the specific immune-mediated destruction of the insulin-producing β-cells of the pancreas. In genetically susceptible individuals, a still undetermined initiating 'hit' triggers a cascade of events that eventually leads to autoreactive CD8 T cells infiltrating the pancreatic islets and, subsequently, destroying them. There is increasing evidence that viruses, especially enteroviruses, are major environmental candidates; however, despite decades of investigation, we still lack certainty with regard to the causation of T1D. Moreover, studies in animal models of diabetes suggest a protective role of certain enteroviral infections upon diabetes contraction, making the quest for viral involvement in T1D even more difficult. Analyzing the foundation and the results of the most current work in the field, this article gives a brief overview of current knowledge, as well as providing an outlook for future directions.

Sirtuins are a class of NAD⁺-dependent deacetylases, such as deacetylases, that have a wide array of biological functions. Recent studies have suggested that reduced sirtuin action is correlated with Type 2 diabetes. Both overnutrition and aging, which are two major risk factors for diabetes, lead to decreased sirtuin function and result in abnormal glucose and lipid metabolism. Therefore, restoring normal levels of sirtuin action in Type 2 diabetes may be a promising method of treating diabetes. This article reviews the biological functions of three of the seven mammalian sirtuins - SIRT1, SIRT3 and SIRT6 - that have demonstrated prominent metabolic roles and early potential for drug targeting. Clinical trials investigating the use of sirtuin activators for treating diabetes are already underway and show promise as alternatives to current diabetes therapies. Thus, further research into sirtuin activators is warranted and may lead to a new class of safe, effective diabetes treatments.

Sirtuins are a group of NAD(+)-dependent enzymes that post-translationally modify histones and other proteins. Among seven mammalian sirtuins, SIRT1 has been the most extensively studied and has been demonstrated to play a critical role in all major metabolic organs and tissues. SIRT1 regulates glucose and lipid homeostasis in the liver, modulates insulin secretion in pancreatic islets, controls insulin sensitivity and glucose uptake in skeletal muscle, increases adiponectin expression in white adipose tissue and controls food intake and energy expenditure in the brain. Recently, SIRT3 has been demonstrated to modulate insulin sensitivity in skeletal muscle and systemic metabolism, and Sirt3-null mice manifest characteristics of metabolic syndrome on a high-fat diet. Thus, it is reasonable to believe that enhancing the activities of SIRT1 and SIRT3 may be beneficial for Type 2 diabetes. Although it is controversial, the SIRT1 activator SRT1720 has been reported to be effective in improving glucose metabolism and insulin sensitivity in animal models. More research needs to be conducted so that we can better understand the physiological functions and molecular mechanisms of sirtuins in order to therapeutically target these enzymes for diabetes treatment.

Over the last decade, our knowledge of β-cell biology has expanded with the use of new scientific techniques and strategies. Growth factors, hormones and small molecules have been shown to enhance β-cell proliferation and function. Stem cell technology and research into the developmental biology of the pancreas have yielded new methods for in vivo and in vitro regeneration of β cells from stem cells and endogenous progenitors as well as transdifferentiation of non-β cells. Novel pharmacological approaches have been developed to preserve and enhance β-cell function. Strategies to increase expression of insulin gene transcription factors in dysfunctional and immature β cells have ameliorated these impairments. Hence, we suggest that strategies to minimize β-cell loss and to increase their function and regeneration will ultimately lead to therapy for both Type 1 and 2 diabetes.

The management of patients with Type 2 diabetes is based on a remarkably robust evidence base. Large clinical trials and lengthy observational cohort studies have clearly established the importance of glycemic, blood pressure and lipid level control. Indeed, most elements of guideline-based diabetes care can be supported by clinical research evidence. While such studies are critical for establishing treatment recommendations, the evidence derived from clinical trial participants applies to populations of patients rather than to the individual sitting before the clinician. An important next step in diabetes care would be to develop and implement a framework for personalizing care. In this article, we highlight the major reasons for personalization and discuss what the future of personalized diabetes care may hold.

Type 2 diabetes and other noncommunicable diseases are a growing public health challenge globally. An estimated 285 million people, corresponding to 6.4% of the world's adult population, has diabetes, which is expected to reach 552 million by the International Diabetes Federation in 2030. A much larger segment of the world's population, approximating 79 million individuals in the USA alone, has prediabetes. Globally, a relatively small percentage of those with diabetes or prediabetes are diagnosed with the potential for developing chronic complications. To address this epidemic, governments, in concert with the private sector, need to set policies that promote healthy nutritional and agricultural policies, favor modifications in the environment that encourage greater physical activity and make prevention affordable for all citizens at high risk. The public health sector has the charge of translating evidence-based findings into practical, accessible and cost-effective programs and monitoring the process to continuously improve prevention initiatives. The clinical sector has the formidable challenge of screening and identifying those at high risk and referring them to accredited intervention programs. There is a need to explore additional cost-effective interventions that are customized to meet individual needs that can be offered at the community and clinical levels. Thus, all three sectors, government, public health and clinical, each have a critical role in this process and by working in a partnership, ought to create the necessary synergies essential for making substantial forays in the prevention of Type 2 diabetes.

A review of national data confirms that while the quality of healthcare in the USA is slowly improving, disparities in diabetes prevalence, processes of care and outcomes for racial/ethnic minorities are not. Many quality measures can be addressed through system level interventions, referred to as quality improvement (QI), and QI collaboratives have been found to effectively improve processes of care for chronic conditions, including diabetes. However, the impact of QI collaboratives on the reduction of health disparities has been mixed. Lessons learned from previous QI collaboratives including the complexity of impacting clinical outcomes, the need for expert support for skills outside of QI methodology, limiting impact of poor data, and the need to develop disparities quality measures, can be used to inform future QI collaborative approaches to reduce diabetes racial/ethnic minority health disparities.

Diabetic ketoacidosis (DKA) has been considered a key clinical feature of Type 1 diabetes mellitus; however, increasing evidence indicates that DKA is also a common feature of Type 2 diabetes (T2DM). Many cases of DKA develop under stressful conditions such as trauma or infection but an increasing number of cases without precipitating cause have been reported in children and adults with T2DM. Such patients present with severe hyperglycemia and ketosis as in Type 1 diabetes mellitus but can discontinue insulin after a few months and maintain acceptable glycemic control on diet or oral agents. This subtype of diabetes has been referred to as ketosis-prone T2DM. In this article, we reviewed the literature on ketosis-prone T2DM and summarized the epidemiology, putative pathophysiology and approaches to management.