Effects of resistance versus aerobic training on coronary artery disease risk factors

Individuals exhibiting "the metabolic syndrome" have multiple coronary artery disease risk factors, including insulin resistance, hyperlipidemia, hypertension, and android obesity. We performed a randomized trial to compare the effects of aerobic and resistance training regimens on coronary risk factors. Twenty-six volunteers who exhibited android obesity and at least one other risk factor for coronary artery disease were randomized to aerobic or resistance training groups. Body mass index, waist-to-hip ratio, glucose, insulin, body composition, 24-hr urinary albumin, fibrinogen, blood pressure, and lipid profile were measured at baseline and after 10 weeks of exercise training. Both groups showed a significant reduction in waist-to-hip ratio and the resistance training group also showed a reduction in total body fat. There was no significant change in mean arterial blood pressure in either group. Fasting plasma glucose, insulin, total cholesterol, low-density lipoprotein (LDL) cholesterol, and triglycerides were unchanged in both groups. High-density lipoprotein (HDL) cholesterol increased (13%) with aerobic training only. Plasma fibrinogen was increased (28% and 34%, P < 0.02) in both groups and both groups showed a significant decrease (34% and 28%, P < 0.03) in microalbuminuria after their respective training regimen. In conclusion, resistance training was effective in improving body composition of middle-aged obese sedentary males. Only aerobic training was effective in raising HDL cholesterol. More studies are warranted to assess the effects of exercise on plasma fibrinogen and microalbuminuria.     

Effects of dietary carbohydrate on the development of obesity in heterozygous Zucker rats

Rats carrying one copy of the fa allele are predisposed to diet-induced metabolic disturbances which contribute to hyperinsulinemia, obesity and dyslipidemia. To investigate the role of dietary carbohydrate and fat in the development of these conditions, we fed 6-week old male heterozygous (fa/+) lean rats carbohydrate-free diets containing primarily saturated fat either ad libitum or pair-fed. These diets were compared to standard chow and to a high saturated fat mixed diet containing 10% energy from sucrose for 4 weeks. The carbohydrate-free diet resulted in significantly lower circulating glucose levels compared to all other groups (p = 0.006). Weight gain was negligible in the carbohydrate free groups compared to standard diet and 10% sucrose diet (p = 0.03). This was reflected in energy efficiency which was markedly reduced (90%) in the carbohydrate-free groups compared to the other groups (p = 0.04). Corresponding changes were noted in fat pad mass. The subscapular and epididymal fat pads were increased 42% and 44%, respectively, in animals consuming the 10% sucrose diet compared to all other groups (p < 0.01). Comparable changes in fatty acid synthase (FAS) mRNA were observed in response to the carbohydrate-free diet, which resulted in a 53% decrease in adipocyte FAS mRNA (p < 0.001). Addition of 10% sucrose to the diet completely reversed this effect resulting in a 69% increase in adipocyte FAS mRNA compared to the carbohydrate-free groups (p = 0.01). Similarly, hepatic FAS mRNA was elevated by 51% and 66% in the 10% sucrose and standard diet groups respectively, compared to the carbohydrate-free groups. Therefore, diets that contain minimal carbohydrate may minimize net lipid storage and adiposity.     

Information processing with population codes

Information is encoded in the brain by populations or clusters of cells, rather than by single cells. This encoding strategy is known as population coding. Here we review the standard use of population codes for encoding and decoding information, and consider how population codes can be used to support neural computations such as noise removal and nonlinear mapping. More radical ideas about how population codes may directly represent information about stimulus uncertainty are also discussed.     

Calcitriol and calcium regulate cytokine production and adipocyte-macrophage cross-talk

OBJECTIVE: The objective of this study was to investigate the effects of calcitriol on adipocyte and macrophage cytokine expression as well as release and on adipocyte-macrophage cross-talk in local modulation of inflammation. RESEARCH PROCEDURES AND RESULTS: We investigated calcitriol modulation of the expression of macrophage inhibitory factor (MIF) and macrophage surface-specific protein CD14, two key factors in regulating macrophage function and survival, in differentiated human adipocytes. Calcitriol significantly increased MIF and CD14 expression by 59% and 33%, respectively, while calcium-channel antagonism with nifedipine completely reversed these effects, indicating that calcitriol stimulates MIF and CD14 expression via a calcium-dependent mechanism. Similar results were also found in cultured 3T3-L1 adipocytes; in addition, calcitriol also up-regulated macrophage colony-stimulating factor, macrophage inflammatory protein, interleukin-6 (IL-6) as well as monocyte chemoattractant protein-1 expression in 3T3-L1 adipocytes and stimulated tumor necrosis factor as well as IL-6 expression in RAW 264 macrophages. These effects were blocked by either a calcium-channel antagonist (nifedipine) or a mitochondrial uncoupler (dinitrophenol). Moreover, co-culture of 3T3-L1 adipocytes with RAW 264 macrophages significantly increased the expression and production of multiple inflammatory cytokines in response to calcitriol in both cell types. CONCLUSIONS: These data demonstrate that calcitriol regulates local inflammation via modulating the interaction between adipocytes and macrophages as well as regulating inflammatory cytokine production in each cell type via calcium-dependent and mitochondrial uncoupling-dependent mechanisms. These data provide further mechanistic explanation for our recent observations that suppression of calcitriol by dietary calcium reduces inflammatory cytokine expression and oxidative stress in adipose tissue.     

Magnesium potentiation of iron-transferrin binding

The binding of iron to transferrin was studied by loading iron (III) onto apotransferrin in a chloride and a nitrilotriacetate form. When magnesium was added, a marked increase occurred in both the rate of iron binding and the maximum level of iron loaded on transferrin utilizing either iron salt. In the absence of magnesium the amount of iron required to achieve 50 percent saturation of the binding sites was 1.6 x 10(-4) M, whereas when magnesium was added, only about one-third as much iron (0.54 x 10(-4) M) was required. These data suggest an allosteric effect on transferrin by magnesium which potentiates iron (III) binding.     

Calcium and dairy product modulation of lipid utilization and energy expenditure

Objective: The purpose of this study was to investigate the impact of dietary calcium or dairy product intake on total energy expenditure (TEE), fat oxidation, and thermic effect of a meal (TEM) during a weight loss trial. Methods and Procedures: The intervention included a prescribed 500‐kcal deficit diet in a randomized placebo‐controlled calcium or dairy product intervention employing twenty‐four 18 to 31‐year‐old (22.2 ± 3.1 years, mean ± s.d.) overweight women (75.5 ± 9.6 kg). TEM and fat oxidation were measured using respiratory gas exchange after a meal challenge, and TEE was measured by doubly labeled water. Fat mass (FM) and lean mass (fat‐free mass (FFM)) were measured by dual‐energy X‐ray absorptiometry. Subjects were randomized into one of these three intervention groups: (i) placebo (<800 mg/day calcium intake); (ii) 900 mg/day calcium supplement; (iii) three servings of dairy products/day to achieve an additional 900 mg/day. Results: There were no group effects observed in change in TEE; however, a group effect was observed for fat oxidation after adjusting for FFM (P = 0.02). The treatment effect was due to an increase in fat oxidation in the calcium‐supplemented group of 1.5 ± 0.6 g/h, P = 0.02. Baseline 25‐hydroxyvitamin D (25OHD) was positively correlated with TEM (R = 0.31, P = 0.004), and trended toward a correlation with fat oxidation (P = 0.06), independent of group assignment. Finally, the change in log parathyroid hormone (PTH) was positively correlated with the change in trunk FM (R = 0.27, P = 0.03). Discussion: These results support that calcium intake increases fat oxidation, but does not change TEE and that adequate vitamin D status may enhance TEM and fat oxidation.