Moises Torres-Gonzalez

Raisins and additional walking have distinct effects on plasma lipids and inflammatory cytokines

BackgroundRaisins are a significant source of dietary fiber and polyphenols, which may reduce cardiovascular disease (CVD) risk by affecting lipoprotein metabolism and inflammation. Walking represents a low intensity exercise intervention that may also reduce CVD risk. The purpose of this study was to determine the effects of consuming raisins, increasing steps walked, or a combination of these interventions on blood pressure, plasma lipids, glucose, insulin and inflammatory cytokines.ResultsThirty-four men and postmenopausal women were matched for weight and gender and randomly assigned to consume 1 cup raisins/d (RAISIN), increase the amount of steps walked/d (WALK) or a combination of both interventions (RAISINS + WALK). The subjects completed a 2 wk run-in period, followed by a 6 wk intervention. Systolic blood pressure was reduced for all subjects (P = 0.008). Plasma total cholesterol was decreased by 9.4% for all subjects (P < 0.005), which was explained by a 13.7% reduction in plasma LDL cholesterol (LDL-C) (P < 0.001). Plasma triglycerides (TG) concentrations were decreased by 19.5% for WALK (P < 0.05 for group effect). Plasma TNF-α was decreased from 3.5 ng/L to 2.1 ng/L for RAISIN (P < 0.025 for time and group × time effect). All subjects had a reduction in plasma sICAM-1 (P < 0.01).ConclusionThis research shows that simple lifestyle modifications such as adding raisins to the diet or increasing steps walked have distinct beneficial effects on CVD risk.

Carbohydrate restriction and dietary cholesterol modulate the expression of HMG-CoA reductase and the LDL receptor in mononuclear cells from adult men

The liver is responsible for controlling cholesterol homeostasis in the body. HMG-CoA reductase and the LDL receptor (LDL-r) are involved in this regulation and are also ubiquitously expressed in all major tissues. We have previously shown in guinea pigs that there is a correlation in gene expression of HMG-CoA reductase and the LDL-r between liver and mononuclear cells. The present study evaluated human mononuclear cells as a surrogate for hepatic expression of these genes. The purpose was to evaluate the effect of dietary carbohydrate restriction with low and high cholesterol content on HMG-CoA reductase and LDL-r mRNA expression in mononuclear cells. All subjects were counseled to consume a carbohydrate restricted diet with 10–15% energy from carbohydrate, 30–35% energy from protein and 55–60% energy from fat. Subjects were randomly assigned to either EGG (640 mg/d additional dietary cholesterol) or SUB groups [equivalent amount of egg substitute (0 dietary cholesterol contributions) per day] for 12 weeks. At the end of the intervention, there were no changes in plasma total or LDL cholesterol (LDL-C) compared to baseline (P > 0.10) or differences in plasma total or LDL-C between groups. The mRNA abundance for HMG-CoA reductase and LDL-r were measured in mononuclear cells using real time PCR. The EGG group showed a significant decrease in HMG-CoA reductase mRNA (1.98 ± 1.26 to 1.32 ± 0.92 arbitrary units P < 0.05) while an increase was observed for the SUB group (1.13 ± 0.52 to 1.69 ± 1.61 arbitrary units P < 0.05). Additionally, the LDL-r mRNA abundance was decreased in the EGG group (1.72 ± 0.69 to 1.24 ± 0.55 arbitrary units P < 0.05) and significantly increased in the SUB group (1.00 ± 0.60 to 1.67 ± 1.94 arbitrary units P < 0.05). The findings indicate that dietary cholesterol during a weight loss intervention alters the expression of genes regulating cholesterol homeostasis.

Carbohydrate restriction and dietary cholesterol distinctly affect plasma lipids and lipoprotein subfractions in adult guinea pigs

To evaluate the effects of carbohydrate restriction (CR) and dietary cholesterol on lipoprotein metabolism, adult male guinea pigs (10 guinea pigs/diet) were fed either low (0.04 g/100 g) or high (0.25 g/100 g) amounts of dietary cholesterol, in combination with either low (10% total energy) or high (54.2% total energy) dietary carbohydrate (control groups) for a total of four groups: high carbohydrate-low cholesterol (control-L), high carbohydrate-high cholesterol (control-H), low carbohydrate-low cholesterol (CR-L) and low carbohydrate-high cholesterol (CR-H). Plasma triglyceride concentrations were lower (P<.01%), while high-density lipoprotein cholesterol concentrations were higher (P<.05) in the CR groups compared to the control groups. In contrast, high dietary cholesterol (CR-H and control-H) resulted in higher concentrations of total and low-density lipoprotein (LDL) cholesterol compared to those guinea pigs fed the low-cholesterol diets (P<.01). Dietary cholesterol significantly increased the total number of LDL particles (P<.001) and the number of small LDL (P<.001), as determined by nuclear magnetic resonance. In contrast, carbohydrate restriction (CR-L and CR-H) resulted in lower concentrations of medium very-low-density lipoprotein and small LDL particles compared to the high-carbohydrate groups. Plasma lecithin:cholesterol acyltransferase (LCAT) activity was decreased and cholesterol ester transfer protein activity was increased by dietary cholesterol, whereas carbohydrate restriction increased LCAT activity (P<.05). These findings are similar to those observed in humans, thus validating the use of adult guinea pigs to study lipid responses to carbohydrate restriction. The results also indicate that the atherogenicity of lipoproteins induced by high dietary cholesterol is attenuated by carbohydrate restriction in guinea pigs.

Replacing dietary carbohydrate with protein and fat decreases the concentrations of small LDL and the inflammatory response induced by atherogenic diets in the guinea pig

Guinea pigs resemble humans in cholesterol and lipoprotein metabolism; however, there is limited information on the vascular inflammatory response with induction of atherosclerosis in this animal model. The purpose of this study was to document a vascular inflammatory response associated with dietary-induced atherosclerosis in the guinea pig and determine the effect of replacing dietary carbohydrate with protein and fat on this response. Thirty male Hartley guinea pigs were randomly assigned to a high dietary cholesterol, high-carbohydrate (HC); a high-cholesterol, low-carbohydrate (LC) or a control (CON) diet for 12 weeks. Analysis of cytokine protein expression [interferon γ (IFN-γ), tumor necrosis factor α (TNF-α), interleukin (IL)-1β, IL-6 and GM-CSF) and m RNA expression (IFN-γ, TNF-α, IL-1β, MCP-1 and IL-8] were performed along with the measurement of cholesterol concentration in the aorta, plasma lipids and plasma low-density lipoprotein subfractions. There was a similar and significant accumulation of cholesterol in the thoracic aorta in the HC and LC groups compared to the CON group. Aortic cytokine protein expression (TNF-α, IFN-γ and IL-6) and m RNA expression (TNF-α and IFN-γ) were significantly elevated in both high-cholesterol fed groups (HC and LC) (P<.05) compared to the CON group. Compared to the HC group, animals fed the LC diet had reduced protein and m RNA TNF-α expression, as well as a reduced concentration of small LDL particles in the plasma. This study is the first to document a dietary cholesterol-induced vascular inflammatory response in guinea pigs that is partially regulated by the macronutrient content of the diet. Guinea pigs may be a useful animal model to evaluate the cellular and molecular components of atherosclerosis.