It is well known that type 2 diabetes mellitus (T2D) is a globally increasing health burden. Despite recent therapeutic advances and the availability of many different classes of antihyperglycemic therapy, a large proportion of people do not achieve glycemic control. A decline in pancreatic beta-cell function has been defined as a key contributing factor to progression of T2D. In fact, a significant proportion of beta-cell secretory capacity is thought to be lost well before the diagnosis of T2D is made. Several models have been proposed to explain the reduction in beta-cell function, including reduced beta-cell number, beta-cell exhaustion, and dedifferentiation or transdifferentiation into other cell types. However, there have been reports that suggest remission of T2D is possible, and it is believed that beta-cell dysfunction may be, in part, reversible. As such, the question of whether beta cells are committed to failure in people with T2D is complex. It is now widely accepted that early restoration of normoglycemia may protect beta-cell function. Key to the successful implementation of this approach in clinical practice is the appropriate assessment of individuals at risk of beta-cell failure, and the early implementation of appropriate treatment options. In this review, we discuss the progression of T2D in the context of beta-cell failure and describe how C-peptide testing can be used to assess beta-cell function in primary care practice. In conclusion, significant beta-cell dysfunction is likely in individuals with certain clinical characteristics of T2D, such as long duration of disease, high glycated hemoglobin (≥9%), and/or long-term use of therapies that continuously stimulate the beta cell. In these people, measurement of beta-cell status could assist with choice of appropriate therapy to delay or potentially reverse beta-cell dysfunction and the progression of T2D.

This synopsis, from the American Diabetes Association Standards of Medical Care, addresses pharmacologic management of type 2 diabetes, including oral and noninsulin injectable therapies, insulin t... Description: The American Diabetes Association (ADA) updates the Standards of Medical Care in Diabetes annually to provide clinicians, patients, researchers, payers, and other interested parties wi...

Vitamin D deficiency has been identified as a common metabolic/endocrine abnormality. Despite known dietary sources of vitamin D and the role of sunlight in its production, much of the US population may have inadequate levels of serum 25-hydroxyvitamin D. Deficiency of vitamin D can be caused by a variety of health conditions, but studies on the effects of vitamin D supplements have had mixed results. This evidence-based clinical review discusses what is currently known about vitamin D and what areas need further research to clarify its role in health and disease.

In the last decade, researchers have gained a greater understanding of the pathophysiologic mechanisms of type 2 diabetes as a chronic and progressive disease. One of the more recent treatment targets is the kidney. The kidneys become maladaptive in diabetes by increasing the reabsorption of glucose above the normal physiologic renal threshold. This discovery has led to the development of the sodium/glucose cotransporter 2 inhibitors (SGLT2). These agents readjust the renal threshold for glucose reabsorption to a lower level and decrease glucose reabsorption, while increasing urinary glucose when the glucose is above the renal threshold and subsequently lowering plasma glucose. The mechanism of action of the SGLT2 inhibitors is insulin independent, which makes them a novel treatment of diabetes. At the time of preparation of this manuscript, there were three SGLT2 inhibitors available in the US. This manuscript focuses on empagliflozin, the newest SGLT2 inhibitor, the trials in its development, and the clinical data available to date. Further, the authors propose future applications of empagliflozin, including in the treatment of type 1 diabetes, and its potential role in renoprotection.

Patients with chronic kidney disease (CKD) and type 2 diabetes (T2D) are at high risk of CKD progression and cardiovascular (CV) disease. Prevalence of CKD in patients with T2D is currently around 40% and continues to grow. The increasing number of people with CKD and T2D will ultimately have a significant impact upon health resource use and costs of care for people with T2D. Management of CKD in patients with T2D aims to preserve kidney function to reduce the risk of end-stage kidney disease, CV events, and mortality. Evidence-based recommendations for the treatment of patients with CKD and T2D are provided by several international and national organizations and recommend several lifestyle and pharmacological approaches to help prevent or delay the progression of CKD in patients with T2D. Guidelines include regular screening of patients with T2D for CKD using spot urine albumin-to-creatinine ratio (UACR) and estimated glomerular filtration rate (at least annually and at least twice a year if UACR >300 mg/g). Additionally, assessment of vascular complications, together with interventions designed to improve glycemic control and lipid levels, maintain healthy body weight, and optimize blood pressure should be performed. Medications shown to slow progression of CKD include renin–angiotensin system inhibitors, sodium-glucose cotransporter-2 inhibitors, glucagon-like peptide 1 receptor agonists, and, more recently, selective, non-steroidal mineralocorticoid receptor antagonists. This review highlights the ongoing challenges facing primary care providers in the management of CKD in patients with T2D including the consideration of comorbidities, adoption of new treatment options, and implementation of individualized care. Achieving consensus for optimal treatment of this disease is critical in providing consistent and appropriate care for all patients. Strategies to improve outcomes should also include use of clear referral criteria, use of a multi-disciplinary approach, and patient education.