Lutein has been shown to be protective against age-related macular degeneration; however, the antiinflammatory and antioxidant effects of this carotenoid in aortas are less known. Guinea pigs were fed a hypercholesterolemic diet (0.25 g cholesterol/100 g) and randomly allocated to a control group (n = 9) or a lutein group (n = 10) (0.01 g/100 g lutein) [corrected] and fed the experimental diets for 12 wk. Plasma LDL cholesterol and TG did not differ between groups; however, the lutein group had lower concentrations of medium size LDL (P < 0.05). As expected, guinea pigs from the lutein group had higher concentrations of plasma and liver lutein than those from the control group (P < 0.0001). Aortic cholesterol and malondialdehyde concentrations were lower in the lutein group (9.6 ± 2.8 mmol/g and 1.69 ± 1.35 nmol/mg protein) compared to the control group (15.5 ± 2.3 mmol/g and 2.98 ± 1.45 nmol/mg protein) (P < 0.05). Hematoxilin and eosin staining indicated that aortas from the control group presented focal intimal thickening, whereas either less thickness or no visible thickness was present in aortas from the lutein group. Oxidized LDL (oxLDL) was lower both in plasma and aorta in the lutein group compared to the control group (P < 0.001). Aortic cytokines were also lower in the lutein group (P < 0.05). Plasma lutein and oxLDL (r = -0.79; P < 0.0001) and plasma lutein and aortic oxLDL (r = -0.64; P < 0.0001) were negatively correlated. These data suggest that lutein exerts potent antioxidant and antiinflammatory effects in aortic tissue that may protect against development of atherosclerosis in guinea pigs.

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Hepatic steatosis is the abnormal retention of lipids in hepatocytes, which can lead to progressive inflammation and fibrosis. Several dietary strategies including the use of low carbohydrate diets have been proposed to ameliorate the metabolic dysregulations caused by hepatic steatosis. Animal models are useful to study diet effects on hepatic lipid accumulation, inflammation and oxidative stress. Guinea pigs are an excellent animal model to study diet effects on cholesterol and lipoprotein metabolism, inflammation and atherosclerosis. The use of guinea pigs as models for hepatic steatosis has not been thoroughly discussed. The purpose of this review is to discuss the metabolic abnormalities that lead to the development of hepatic steatosis, to review some dietary treatments that can reverse these abnormalities and finally to propose the guinea pig as an animal model to study the metabolic pathways, signaling and genetic mechanisms associated with hepatic steatosis and non-alcoholic fatty liver disease.

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BACKGROUND/OBJECTIVESThe main objective of this study was to evaluate the effects of a high cholesterol (HC) dietary challenge on cholesterol tissue accumulation, inflammation, adipocyte differentiation, and macrophage infiltration in guinea pigs. A second objective was to assess whether macronutrient manipulation would reverse these metabolic alterations.MATERIALS/METHODSMale Hartley guinea pigs (10/group) were assigned to either low cholesterol (LC) (0.04g/100g) or high cholesterol (HC) (0.25g/100g) diets for six weeks. For the second experiment, 20 guinea pigs were fed the HC diet for six weeks and then assigned to either a low carbohydrate (CHO) diet (L-CHO) (10% energy from CHO) or a high CHO diet (H-CHO) (54% CHO) for an additional six weeks.RESULTSHigher concentrations of total (P < 0.005) and free (P < 0.05) cholesterol were observed in both adipose tissue and aortas of guinea pigs fed the HC compared to those in the LC group. In addition, higher concentrations of pro-inflammatory cytokines in the adipose tissue (P < 0.005) and lower concentrations of anti-inflammatory interleukin (IL)-10 were observed in the HC group (P < 0.05) compared to the LC group. Of particular interest, adipocytes in the HC group were smaller in size (P < 0.05) and showed increased macrophage infiltration compared to the LC group. When compared to the H-CHO group, lower concentrations of cholesterol in both adipose and aortas as well as lower concentrations of inflammatory cytokines in adipose tissue were observed in the L-CHO group (P < 0.05). In addition, guinea pigs fed the L-CHO exhibited larger adipose cells and lower macrophage infiltration compared to the H-CHO group.CONCLUSIONSThe results of this study strongly suggest that HC induces metabolic dysregulation associated with inflammation in adipose tissue and that L-CHO is more effective than H-CHO in attenuating these detrimental effects.