By Louis Kuritzky, MD, Clinical Assistant Professor, University of Florida, Gainesville. Dr. Kuritzky is a consultant for Sucampo Pharmaceuticals, Takeda, Boehringer Ingelheim; and is a consultant and on the speaker's bureau for Novo Nordisk, Lilly, Daiichi Sankyo, Forest Pharmaceuticals, Cephalon, Novartis, and Sanofi Aventis.
Female sexual dysfunction in diabetes
Source: Esposito K, et al. Int J Impot Research 2010;22:179-184.
Male sexual dysfunction is well recognized as a consequence of diabetes. Currently, there are no approved medications for treatment of female sexual dysfunction (FSD), though epidemiologic surveys suggest that the population prevalence of FSD rivals that of male sexual dysfunction. FSD is typically categorized as either disorders of desire, arousal, orgasm, or pain. Of course, FSD subcategories are commonly comorbid.
This study recruited adult type 2 diabetic women (mean age, 58 years) attending a clinic in Italy for routine care of diabetes to complete the Female Sexual Function Index, a validated instrument for assessing FSD.
Overall, the prevalence of FSD in the entire population was 53%. This is similar to, but greater than, the prevalence reported in 2 large population surveys (both with broader age range, and not limited to diabetics), which indicated an FSD prevalence of 43%. FSD was 30% more frequent in postmenopausal women than premenopausal women and was associated with depression. The only recognized protective factor was physical activity.
The etiology of FSD in diabetes is unclear, and may include vascular, neurologic, and endocrinologic factors. The high prevalence of FSD in diabetic women should motivate clinicians to be more proactive in its identification.
Exenatide + rosiglitazone added to metformin
Source: DeFronzo RA, et al. Diabetes Care 2010;33:951-957.
It is widely recognized that approximately half of beta-cell function (BCF) has been lost by the time type 2 diabetes (DM2) is diagnosed. Additionally, it appears that despite vigorous treatment, loss of BCF continues inexorably.
The most recently published treatment algorithm for DM2 management by the ADA suggests that initial therapy should be lifestyle with metformin, unless a specific contraindication to metformin exists. Over time, however, most patients will require augmentation of treatment.
Exenatide (EXE) and rosiglitazone (ROS) are effective therapies for glucose control and work by complementary mechanisms of action. Additionally, sometimes thiazolidinedione therapy is compromised by weight gain, but since EXE consistently provides weight loss, their combination is clinically sensible.
DM2 subjects already on treatment with lifestyle + metformin (n = 101) were randomly assigned to add-on therapy with EXE alone, ROS alone, or EXE + ROS, and followed for 20 weeks. BCF was measured by the glucose disposition index.
In addition to the anticipated reduction in A1c by polypharmacy, EXE + ROS provided significant improvements in insulin secretion and overall BCF. Long-term studies are necessary to discern whether these favorable effects can be sustained and translated into risk reduction for macro- and/or microvascular outcomes.
Dietary added sugar and lipids
Source: Welsh JA, et al. JAMA 2010; 303:1490-1497.
Processed foods often contain added sucrose or high-fructose corn syrup to enhance palatability. Such added sugars (aSUG) may comprise as much as 16% of Americans' caloric intake. The Institute of Medicine suggests a 25% maximum of daily calories from aSUG and the American Heart Association suggests a 5% maximum. The incidence of obesity, diabetes, and dental caries is associated with increased aSUG, but the relationship between aSUG and lipids is less well- defined.
Welsh et al studied the relationship between aSUG and lipids in NHANES participants (n = 6113). Overall, approximately 16% of calories daily were supplied by aSUG in this population of adults. Excluded from analysis were persons with dietary reports that appeared unreliable (e.g., < 600 calories/day), marked triglyceride elevation, BMI > 65 kg/m2, and those taking cholesterol-lowering medications.
There was a statistically significant association between progressively higher levels of aSUG and lower HDL. Similarly, LDL and triglyceride levels were linearly related to aSUG, although the LDL results were not statistically significant in men.
The mechanism(s) by which aSUG consumption is related to lipid levels is incompletely understood, although it is recognized that fructose may stimulate hepatic lipid production and reduce peripheral lipid clearance. Although not demonstrated in a clinical trial, conceptually, reductions in aSUG on a population-wide basis could have important public health benefits.