Blood pressure (BP) variability (BPV) contributes to target organ damage independent of BP. The authors examined the effect of a 1-year multidisciplinary intervention on BPV in patients with the metabolic syndrome (MetS) as defined by criteria from the Third Report of the Adult Treatment Panel. Forty-four nondiabetic patients underwent clinical and biochemical profiling, 24-hour ambulatory BP monitoring (ABPM), body composition, carotid intima-media thickness, and carotid-femoral pulse wave velocity (PWV). The intervention targeted all MetS components. BPV was assessed by the standard deviation of daytime systolic BP derived from ABPM. Patients with low and high BPV (lower or higher than the median daytime standard deviation of 11.6 mm Hg) did not differ in regards to systolic and diastolic BP, age, fasting glucose, glycated hemoglobin, and body mass index, but the high-variability group had higher values of low-density lipoprotein and leg fat. The 1-year intervention resulted in weight reduction but not BP-lowering. BPV declined in the high-variability group in association with lowering of PWV, C-reactive protein, glycated hemoglobin, alanine aminotransferase, asymmetric dimethylarginine, and increased high-density lipoprotein cholesterol. A multidisciplinary intervention independent of BP-lowering normalized BPV, lowered PWV, and enhanced metabolic control. J Clin Hypertens (Greenwich). 2016;18:19-24. ª 2015 Wiley Periodicals, Inc.Blood pressure (BP) is characterized by marked short-term fluctuations such as beat-to-beat, minuteto-minute, hour-to-hour, and day-to-night changes. Twenty-four-hour ambulatory BP monitoring (ABPM) is the most widely available tool to assess short-term BP variability (BPV) and its wide use in the practice and research of hypertension allows meaningful insight into BPV's patterns, clinical significance, and underlying mechanisms. It is well-accepted that short-term (within 24 hours) variations are affected by sympathetic activation, peripheral resistance (caused by arterial elastic properties), 1-3 blood viscosity, vasoconstrictors effects, and emotional and behavioral factors. There is also growing appreciation that BPV contributes to cardiovascular (CV) complications such that increased variability amplifies the damage caused by high BP per se. BPV likely comprises an independent predictor of CV mortality in the general population, as well as among hypertensive patients.4-6 Interestingly, little is known about the relationship between the metabolic syndrome (MetS) in nondiabetic patients and BPV. Although the MetS is common in patients with hypertension, and hypertension is a key component of the MetS, certain obesity-related features of the MetS are not an essential part of the hypertensive phenotype in the general population. Furthermore, the MetS embodies one example of hypertension, in which the treatment of high BP does not necessarily comprise the major therapeutic target, but is rather one of several concomitant interventions to curb overall risk factor control. From an inve...
Background: In the treatment of obesity/metabolic syndrome, dietary measures traditionally focus on reducing carbohydrate/fat-related caloric intake. The possibility that changes in potassium consumption may be related to the achieved weight loss has not been previously explored. Methods: Sixty-eight participants, with a mean age of 51.6 ± 11.0 years (F/M—30/38), who fulfilled the ATPIII criteria for the metabolic syndrome (MS) were enrolled into a 1-year intensive multidisciplinary program. Nutritional recommendation consisted of a moderate low calorie/high protein Mediterranean diet. Baseline assessment included clinical and biochemical profiling, and body composition. Nutritional components were registered over 7 days before and at the end of 1 year of treatment. Results: Mean baseline body mass index (BMI) was 35 ± 4 kg/m², which declined by 9.4 ± 0.1% after one year of combined intervention. Linear stepwise regression analysis revealed that 45% of the predicted variance of the % decline in BMI was related to increased consumption of dietary potassium (β = −0.865) and caproic acid (β = −0.423) and reduction in the consumption of dietary vitamin B6 (β = 0.542), calcium (β = 0.335), total carbohydrates (β = 0.239) and total caloric intake (β = 0.238; p < 0.001). Notably, the strongest correlate of the decline in BMI was the increase in dietary potassium intake (β = −0.865). Subjects whose achieved decrease in BMI was above the average (n = 30) increased potassium intake by 25% as compared to an increase in dietary potassium intake of only 3% by those whose decline in BMI was below the average (n = 36; p < 0.05). The change in dietary potassium was related to the percent increase in dietary protein (r = 0.433; p < 0.001). Conclusion: An increase in dietary potassium consumption is a previously unrecognized predictor of the achieved reduction in BMI in a weight-loss-oriented multidisciplinary intervention in obesity/MS. Prospective trials are underway to confirm this post-hoc finding.
Background: With the growing prevalence of obesity, there is also a rise in the incidence of metabolic syndrome (MS). It is characterizes by hyperinsulinemia, increased fasting glucose, hypertriglyceridemia, low HDL, increased waist circumference and hypertension.Insulin-degrading enzyme (IDE) is the major enzyme responsible for insulin degradation among other proteins linked to glucose metabolism such as glucagon. Using genome wide associated studies, IDE was identified as a diabetes susceptibility gene. Furthermore, inhibition of IDE was suggested as therapeutic target for type 2 diabetes. Objectives: Study the difference in IDE levels between healthy and MetS subjects. Characterize metabolic parameters which correlate with IDE.Explore IDE levels in a mouse model of obesity/ insulin resistance. Methods: We developed highly specific anti IDE antibodies with the ability to detect human IDE levels using ELISA. IDE levels were measured in 45 MS subjects and 30 controls. Results: As expected, MS subjects had higher BMI, glucose, triglycerides and insulin levels, with lower HDL levels. IDE levels were higher in MS subjects (average 692 +/-464 vs 420 +/- 232 pg/microliter; p<0.01). We also found a strong correlation between IDE levels and triglyceride levels (r= 0.305; p<0.05), and negative correlation with HDL levels (r= -0.347; p<0.05). This difference remained significant even after multi-variant analysis.Of interest, IDE levels in MS subjects were clearly segregated into two different subgroups, subjects with "normal IDE", with value distribution and mean (n=25; 278+/-156 pg/ul) which were indistinguishable from the normal control group and subjects with high IDE (n=25; 1272+/-757 pg/ul<0.001 for the difference between normal and high IDE). The high IDE MS group was older and had higher glucose levels than the normal IDE MS group (54 +/- 10 vs 45+/-13 years; p=0.01; and (94+/-20 vs 80+/-8 mg/dl; p=0.01; respectively). Conclusions: IDE is higher in MS subjects and is related to age and fasting glucose. Whether or not this is a compensatory mechanism or contributes to disease progression remains to be explored. Unless otherwise noted, all abstracts presented at ENDO are embargoed until the date and time of presentation. For oral presentations, the abstracts are embargoed until the session begins. Abstracts presented at a news conference are embargoed until the date and time of the news conference. The Endocrine Society reserves the right to lift the embargo on specific abstracts that are selected for promotion prior to or during ENDO.
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