OBJECTIVETo know whether age has an independent effect on the dawn phenomenon in noninsulin-using type 2 diabetes.RESEARCH DESIGN AND METHODSEighty-one individuals with type 2 diabetes were matched for HbA1c and divided by age into three subgroups of 27 individuals (1: ≥70 years; 2: 60–69 years; and 3: ≤59 years). All underwent ambulatory continuous glucose monitoring for quantifying the dawn phenomenon (i.e., the absolute [∂G, mg/dL] or relative [∂G%] increments from nocturnal nadirs to prebreakfast time points).RESULTSHbA1c levels and 24-h glycemic profiles were similar across the three groups. Glucose increments (mean ± SEM) were identical in the three groups: ∂G (mg/dL), 22.0 ± 4.7 (1), 21.3 ± 3.6 (2), and 18.0 ± 3.6 (3) and δG (%), 19.9 ± 4.9 (1), 21.6 ± 4.4 (2), and 17.6 ± 4.2 (3). Using the most common definition (∂G >10 mg/dL), the prevalence of the dawn phenomenon was 52, 70, and 59% in groups 1, 2, and 3, respectively.CONCLUSIONSThe dawn phenomenon is present in the elderly.
In subjects with SCH at the early phase of TSH-suppressive therapy, evidence of isolated longitudinal LV diastolic dysfunction was observed, despite a normal LV morphology. Further prospective studies to clarify the prognosis of picking-up early diastolic dysfunction in asymptomatic patients are needed before serial measurements could be recommended.
Insulin resistance is the main factor involved in the occurrence of the metabolic syndrome and later development of type2 diabetes. Despite decades of research on hormone's target tissues and the identification of most diverse candidates, the factors responsible for insulin resistance are still largely undefined. There is also a large discrepancy between in vitro and in vivo insulin sensitivity. Finally it is increasingly demonstrated that insulin resistance is found very early in life, long before metabolic syndrome is established. In search for commonalities, this book deals therefore with a new hypothesis considering microcirculation as one prime, possibly causal effector of insulin resistance. To present this novel hypothesis, the specificities of microvascular physiological mechanisms and the limits of interpretations of data according to the measurement techniques used are first thoroughly described. Several chapters deal with experimental and clinical investigations showing the involvement of microcirculation in insulin resistance. This book provides sound support for microcirculation being linked to insulin resistance at least in a bidirectional way. Supportive evidence suggests that microvascular dysfunction may lie upstream of insulin resistance in many of them. While this is still a hypothesis, the authors believe that there is enough data supporting it and hope that this book will stimulate researchers to provide the necessary final proofs.
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