Change in Hemoglobin A1c and Quality of Life with Real-Time Continuous Glucose Monitoring Use by People with Insulin-Treated Diabetes in the Landmark Study.

Background: Initiating continuous glucose monitoring (CGM) can affect hemoglobin A1c (HbA1c) levels and patients' relationship with their diabetes. We used real-world HbA1c data to quantify short-term changes in glycemia and validated psychosocial questionnaires to assess changes in quality-of-life indicators in people during their first few months of CGM use. Methods: Eligibility was assessed during calls to Dexcom sales regarding its G6 CGM System. Eligibility criteria included ages 25-65 years, type 1 (T1D) or type 2 diabetes (T2D) on intensive insulin therapy (IIT), and no prior CGM use. Participants used a web-based portal to complete the 17-item Diabetes Distress Scale (DDS) and the 14-item Hypoglycemia Attitudes and Behavior Scale (HABS); provided validated HbA1c measurements; and shared their CGM data pre- and 3-5 months post-CGM initiation. Satisfaction and ease of use with the G6 System were also assessed. Results: Data were available from 248 patients (182 with T1D, 66 with T2D; 57% male, 88% non-Hispanic white). Mean (standard deviation) HbA1c fell significantly from 8.2% (1.9%) at baseline to 7.1% (1.1%) at the end of the study (P < 0.001); more than half (54.4%) of those with initial HbA1c values >7% experienced absolute HbA1c reductions of >1%. Significant reductions in diabetes distress (DDS) and hypoglycemic concerns (HABS) were observed (P < 0.001). Most (93%) participants were satisfied or very satisfied with the G6 System and 73% found it very easy to use. Conclusions: The first 3 months of CGM use was correlated with improvements in psychosocial outcomes and improved HbA1c levels for people with T1D or T2D who use IIT.

Effect of aging on fatty streak formation in a diet-induced mouse model of atherosclerosis.

Age is considered to be a major risk factor for atherosclerosis, but it is unclear whether age has a direct effect on susceptibility to atherosclerosis. Wild-type mice develop fatty streak lesions in the aortic root only when fed a cholate-containing high fat/cholesterol diet. To investigate the influence of age on fatty streak formation, young (10 weeks) and old (53 weeks) female C57BL/6 mice were fed an atherogenic diet containing 15% fat, 1.25% cholesterol and 0.5% sodium cholate for 12 weeks. Atherosclerotic lesions at the aortic root were measured after cryosections were stained with oil red O. Results showed that old mice developed a comparable size of aortic lesions with young counterparts (5,600 +/- 2,480 vs. 6,457 +/- 1,537 microm2/section; p = 0.77), although old mice had significantly higher plasma cholesterol levels than young mice on the atherogenic diet (p < 0.05). Plasma levels of soluble vascular cell adhesion molecule 1 were significantly higher in old mice than in young mice on both chow and Western diets (p < 0.005). These data indicate that age has no direct effect on atherosclerosis susceptibility although it is accompanied by elevations in plasma cholesterol and vascular cell adhesion molecule 1 levels in C57BL/6 mice. Thus, increased cardiovascular events with age are probably related to a progressive increase in plaque size rather than to an increase in atherosclerosis susceptibility.

Quantitative trait locus analysis of carotid atherosclerosis in an intercross between C57BL/6 and C3H apolipoprotein E-deficient mice.

BACKGROUND AND PURPOSE: Inbred mouse strains C57BL/6J (B6) and C3H/HeJ (C3H) exhibit marked differences in atherosclerotic lesion formation in the carotid arteries on the apolipoprotein E-deficient (apoE(-/-)) background when fed a Western diet. Quantitative trait locus analysis was performed on an intercross between B6.apoE(-/-) and C3H.apoE(-/-) mice to determine genetic factors contributing to variation in the phenotype. METHODS: Female B6.apoE(-/-) mice were crossed with male C3H.apoE(-/-) mice to generate F(1) hybrids, which were intercrossed to generate 241 female F(2) progeny. At 6 weeks of age, F(2) mice were started on a Western diet. After being fed the diet for 12 weeks, F(2) mice were analyzed for phenotypes such as lesion size in the left carotid arteries and plasma lipid levels and typed for 154 genetic markers spanning the mouse genome. RESULTS: One significant quantitative trait locus, named CAth1 (25 cM, log of the odds score: 4.5), on chromosome 12 and 4 suggestive quantitative trait loci, on chromosomes 1, 5, 6, and 11, respectively, were identified to influence carotid lesion size. One significant quantitative trait locus on distal chromosome 1 accounted for major variations in plasma low-density lipoprotein/very-low-density lipoprotein, high-density lipoprotein cholesterol, and triglyceride levels. Carotid lesion size was not significantly correlated with plasma low-density lipoprotein/very-low-density lipoprotein or high-density lipoprotein cholesterol levels. CONCLUSIONS: These data indicate that the loci for carotid lesions do not overlap with those for aortic lesions as identified in a previous cross derived from the same parental strains, and carotid atherosclerosis and plasma lipids are controlled by separate genetic factors in the B6 and C3H mouse model.