1,721,010 research outputs found
Thirty years of research on the dawn phenomenon: lessons to optimize blood glucose control in diabetes.
No full textMore than 30 years ago in Diabetes Care, Schmidt et al. (1) defined “dawn phenomenon,” the night-to-morning elevation of blood glucose (BG) before and, to a larger extent, after breakfast in subjects with type 1 diabetes (T1D). Shortly after, a similar observation was made in type 2 diabetes (T2D) (2), and the physiology of glucose homeostasis at night was studied in normal, nondiabetic subjects (3–5). Ever since the first description, the dawn phenomenon has been studied extensively with at least 187 articles published as of today (6). In this issue, Monnier et al. (7) report an additional observation on the dawn phenomenon in a large group of T2D subjects and quantify its role on overall BG control. Given this information and the extensive data to date, an assessment of our knowledge in this area should be determined. Specifically, what have we learned from the last 30 years of research on the dawn phenomenon? What is the appropriate definition, the identified mechanism(s), the importance (if any), and the treatment of the dawn phenomenon in T1D and T2D
[Usefulness of plantar pressure measurement for the prevention and treatment of neuropathic diabetic foot].
No full textA disease of the legs, and more specifically of the feet, is a frequent occurrence in diabetic patients and can lead to the major risk of amputation. The pathogenesis of this disease is complex and due to vascular damage and neuropathy. The neuropathic ulcer is a typical clinical manifestation of the "diabetic foot". The pathogenesis of this manifestation is discussed. The most important thing is to prevent this disease. The diabetologist must regularly examine the feet of the patients and measure the foot pressure. We discuss a new instrument, the Dynamic System, which we believe of great help to diabetologist in measuring the foot pressure of diabetic patients
Real-time continuous glucose monitoring decreases the risk of severe hypoglycemia in people with type 1 diabetes and impaired awareness of hypoglycemia
No full textHypoglycemia in persons with type 1 diabetes (T1DM) is the consequence of the insulin therapy necessary to control hyperglycemia and prevent its long-term complications. Hypoglycemia also, however, has important clinical consequences, as it is a risk factor for morbidity and mortality and heavily impacts the quality of life of people with diabetes. Unquestionably hypoglycemia contributes to increased health expenditures. Prevention of the risk of hypoglycemia must be one of the main objectives in the treatment of diabetes, especially if the glycemic target is ambitious
Ipoglicemia: Implicazioni cliniche e impatto sulla salute
No full textHypoglycemia: clinical implications and impact on health
Hypoglycemia in persons with diabetes has a iatrogenic cause,
inducing recurrent symptomatic and sometimes disabling
episodes, involving several organs and systems. Iatrogenic hypoglycemia
has a heavy impact on a patient’s quality of life and
is the main barrier to the implementation of intensive treatment
from both the physician’s and the patient’s perspective, precluding
the full achievement of the potential benefits of good
glycemic control. The challenge for patients and doctors is to
achieve a fine balance between near-normal glucose control
and minimal risk of hypoglycemia. This goal can be achieved if
doctors and patients, with their different clinical needs, are continually
educated about making the best use of insulin and/or
oral drugs
GLP-1 RAs as compared to prandial insulin after failure of basal insulin in type 2 diabetes: Lessons from the 4B and Get-Goal DUO 2 trials
No full textThe add-on of a prandial (short-acting) GLP-1 RA to basal insulin in subjects with T2DM who fail to control A1C on basal insulin, stems from the physiological principles of post-prandial glucose homeostasis, and it is based on evidence from clinical trials. The 4B and GetGoal DUO 2 studies are the first to establish in head-to-head comparison, the efficacy and safety of short-acting GLP-1 RAs vs prandial insulin, when added-on to basal insulin glargine. In the 4B study (exenatide 2/d vs lispro 3/d) exenatide demonstrated similar efficacy vs lispro in reducing A1C to ~7.2%. However, exenatide reduced also body weight and hypoglycemia incidence as compared to lispro. In GetGoal DUO 2, the head-to-head comparison was between lixisenatide 1/d vs glulisine either 1/d (at the main meal, basal-plus) or 3/d (basal-bolus). Like in 4B, in GetGoal DUO 2 the A1C decreased to similar values with lixisenatide or glulisine 1/d (~7.2%), or glulisine 3/d (~7.0%). Again, as in the 4B, body weight and hypoglycemia incidence were lower with lixisenatide. In both studies a similar percentage of subjects reached the A1C <7.0% on GLP-1 RA or prandial insulin. A higher percentage of subjects reported adverse events on GLP-1 RAs, primarily gastrointestinal related. The studies 4B and GetGoal DUO 2 suggest that after failure of basal insulin in T2DM, the add-on of prandial GLP-1 RA is as effective as prandial insulin in lowering A1C, with added benefits of reducing body weight and risk for hypoglycemia. In addition, the GLP-1 RA + basal insulin is a simpler therapeutic option as compared to basal-plus and basal-bolus regimens
Superiority of insulin analogues versus human insulin in the treatment of diabetes mellitus.
No full textThe modern goals of insulin replacement in Type 1 and Type 2 diabetes mellitus (T1, T2DM) are A1C <6.5% long-term, and prevention of hypoglycaemia (blood glucose, BG <70 mg/dl). In addition to appropriate education and motivation of diabetic subjects, the use of rapid- and long-acting insulin analogues, is critical to achieve these goals. The benefits of rapid-acting analogues (lispro, aspart and glulisine have similar pharmacodynamic effects) compared with non-modified human regular insulin, are: (a) lower 1- and 2-h post-prandial blood glucose; (b) lower risk of late post-prandial hypoglycaemia (and therefore lower BG variability); (c) better quality of life (greater flexibility in timing and dosing of insulin). In T1DM, rapid-acting analogues improve A1C only by the extent to which replacement of basal insulin is optimized at the same time, either by multiple daily NPH administrations, or continuous subcutaneous insulin infusion (CSII), or use of the long-acting insulin analogues glargine or detemir. In T2DM, rapid-acting analogues reduce post-prandial hyperglycaemia more than human regular insulin, but systematic studies are needed to examine the effects on A1C. The benefits of long-acting insulin analogues glargine and detemir vs. NPH, are: (1) lower fasting BG combined with lower risk of hypoglycaemia in the interprandial state (night); (2) lower variability of BG. Glargine and detemir differ in terms of potency and duration of action. Detemir should be given twice daily in the large majority of people with T1DM, and in a large percentage of subjects with T2DM as well, usually at doses greater vs those of the once daily glargine. However, when used appropriately for individual pharmacokinetics and pharmacodynamics, glargine and detemir result into similar effects on BG, risk of hypoglycaemia and A1C. Rapid- and long-acting insulin analogues should always be combined in the treatment of T1 and T2DM
Pivotal Role of Timely Basal Insulin Replacement After Metformin Failure in Sustaining Long-Term Blood Glucose Control at a Target in Type 2 Diabetes
No full textType 2 diabetes over time associates with the development of vascular complications (1). The causative role of long-term elevation of blood glucose is well established, at least for microvascular complications, since intervention strategies directed at reducing hyperglycemia lower onset and/or progression of microangiopathy (1,2). The role of hyperglycemia and its treatment in the development of macrovascular complications is less well established. In fact, it takes a longer time to observe a positive effect of better blood glucose control (in addition to reducing the multiple risk factors often associated with type 2 diabetes such as hypertension, visceral obesity, and hyperdyslipidemia) on macroangiopathy compared with microangiopathy (1,3,4). Today’s understanding of the complex relationship between hyperglycemia and complications in type 2 diabetes predicates that only an early and aggressive blood glucose–lowering intervention (in addition to reduction of the above mentioned risk factors), successfully sustained over time, will translate into benefits on macrovascular complications several years later (likely 10–15 years) (1,3–5). Thus, the present recommendation is to intensively treat people with type 2 diabetes from the clinical onset of the disease, particularly subjects with short diabetes duration who likely have not yet developed vascular complications and who presumably have a long life-expectancy (6).
At present, the question is not whether to intensively treat people with type 2 diabetes at onset of the disease to prevent long-term complications. The question rather is how to intensively treat type 2 diabetes over the many years and decades of the progression of the disease to consistently keep A1C levels <7.0% over the entire cycle of type 2 diabetes. At present, this question is difficult to answer, primarily because of the lack of evidence of long-term effects of one specific intervention, compared with several other possible intervention strategies (7) in type 2 diabetes. In addition, one should always keep in mind that type 2 diabetes is a complex disease characterized by large heterogeneity among individuals and variable progression over time that may eventually result in a nearly total loss of pancreatic β-cell function in just a few years (8,9)
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