Current Diabetes Reviews - Volume 6, Issue 3, 2010

As older adults make up an increasingly lager proportion of the diabetic population, the spectrum of chronic diabetes complications will change and expand. Aside from the traditional long-term complications, diabetes has been associated with excess risk of a number of clinical conditions typical of the geriatric population, including functional decline, physical disability, falls, fractures, cognitive impairment and depression. These conditions are common and profoundly affect the quality of life of older patients with diabetes. The identification of effective ways of preventing and treating these emerging complications, thus improving quality of life among older diabetic patients, is already a major issue in geriatric medicine. In this narrative review, we describe current epidemiological and clinical evidence supporting the association between diabetes and physical disability in older persons. Furthermore, the potential biological mechanisms underlying such an association are analyzed.

The relationship between diabetes and bone disease is complex. While low bone mineral density (BMD) is consistently observed in type 1 diabetes (T1DM), in type 2 diabetes (T2DM) bone mineral density is similar to or higher than in non diabetic subjects. Yet, for both types of diabetes bone appears to be more fragile for a given density. Recent meta-analyses and cohort studies confirm that T1DM and T2DM are associated with higher fracture risk. Many factors influence the probability of fractures. Diabetes can affect bone through multiple pathways including obesity, changes in insulin levels, higher concentrations of advanced glycation end products in collagen, increased urinary excretion coupled with lower intestinal absorption of calcium, inappropriate homeostatic response of parathyroid hormone secretion, complex alterations of vitamin D regulation, reduced renal function, lower insulin-like growth factor-I, microangiopathy, and inflammation. Data on cellular mechanisms and experimental models are extensive, but the relevance of each one of these factors to the clinical situation is unclear. In this article we review the pathophysiological mechanisms potentially involved in the altered BMD found in diabetic patients, show data on the increased risk of fractures, and speculate on the potential causes of the increased risk of fractures in this context. Finally, we comment on the prevention and treatment of osteoporosis in diabetes, although the lack of trials testing the use of pharmacotherapy on preventing fractures in this context is emphasized.

Obstructive Sleep Apnoea Syndrome (OSAS) is a common disorder, characterised by repetitive episodes of partial or complete obstruction of the upper airway during sleep and associated with increasing respiratory efforts. These perturbations lead, in turn, to oxyhaemoglobin desaturation, sleep fragmentation, and daytime symptoms, mainly excessive sleepiness. Accumulating evidence suggests that intermittent hypoxia and oxyhaemoglobin desaturation may result, independently of obesity, in impaired glucose metabolism, as well as insulin resistance even in non-diabetic patients with OSAS. Additionally, OSAS has been proposed as an independent risk factor for type 2 diabetes mellitus. Continuous Positive Airway Pressure (CPAP) is the treatment of choice for OSAS, since it eliminates upper airway collapse during sleep and also improves sleep fragmentation, daytime symptoms and quality of life. Moreover, it has been proposed that the amelioration of breathing disturbances during sleep can improve several markers of glucose metabolism and insulin resistance, such as glycated haemoglobin, fasting glucose, insulin, and insulin resistance. Indeed, some studies have reported improvements in these parameters especially in compliant patients. However, other works failed to confirm this beneficial effect. The present article reviews the issue whether CPAP treatment exerts a beneficial effect on glucose metabolism and insulin resistance.

Nonadherence to different aspects of the diabetes regimen is common. Problems early in the course of illness predict later difficulties with nonadherence; conversely, good management early on protects against later complications. Screening for early risk factors at the time of diabetes diagnosis is therefore critical for promoting the health of children with type 1 diabetes. The purpose of this paper is to review and synthesize the recent empirical literature on early risk factors for nonadherence in type 1 diabetes, with a focus on three specific adherence behaviors: insulin administration, blood glucose monitoring, and clinic attendance. Risk factors are considered within several broad categories: sociodemographic barriers that limit access to care; child and parent factors that affect adherence both directly and indirectly via their impact on the development of family teamwork; and family interactions with their health-care providers. We integrate the different findings into a “simple model” that can be used to develop efficient screening protocols that can in turn guide efforts at preventive intervention.

Diabetes remains a major burden. More than 200 million people are affected worldwide, which represents 6% of the population. The success achieved over the last decade with islet transplantation suggests that diabetes can be cured by the replenishment of deficient beta cells. These observations are proof-of-concept and have intensified interest in treating diabetes not only by cell transplantation but also by stem cells. Regeneration of beta cells from stem and progenitor cells is an attractive method to restore islet cell mass. Pancreatic stem/progenitor cells have been identified, and the formation of new beta cells from pancreatic duct, acinar and liver cells is an active area of investigation. Protocols for the in vitro differentiation of embryonic stem (ES) cells based on normal developmental processes have generated beta-like cells that produce high levels of insulin, even though at low efficiency and without full responsiveness to extracellular levels of glucose. Induced pluripotent stem (iPS) cells can also yield insulin-producing cells following similar approaches. Some agents including glucagon-like peptide-1/exendin-4 can stimulate the regeneration of beta cells in vivo as well as in vitro. Overexpression of embryonic transcription factors in stem cells could efficiently induce their differentiation into insulin-expressing cells. Recent progress in the search for new sources of beta cells has opened up several possibilities for the development of new treatments for diabetes.