Summary The aim of this study was to investigate the effect of dietary lemon polyphenols on high-fat diet-induced obesity in mice, and on the regulation of the expression of the genes involved in lipid metabolism to elucidate the mechanisms. Mice were divided into three groups and fed either a low fat diet (LF) or a high fat diet (HF) or a high fat diet supplemented with 0.5% w/w lemon polyphenols (LP) extracted from lemon peel for 12 weeks. Body weight gain, fat pad accumulation, the development of hyperlipidemia, hyperglycemia, and insulin resistance were significantly suppressed by lemon polyphenols. Supplementation with lemon polyphenols also significantly up-regulated the mRNA level of the peroxisome proliferator activated receptor-α (PPARα) compared to the LF and HF groups in the liver. Furthermore, the mRNA level of acyl-CoA oxidase (ACO) was up-regulated in the LP group compared to the LF group, but not HF group in the liver, and was also significantly increased in the epididymal white adipose tissue. Thus, feeding with lemon polyphenols suppressed body weight gain and body fat accumulation by increasing peroxisomal β-oxidation through upregulation of the mRNA level of ACO in the liver and white adipose tissue, which was likely mediated via up-regulation of the mRNA levels of PPARα.

Several lines of evidence have demonstrated that C-reactive protein (CRP) is associated with oxidative stress; however, the precise co-localization between CRP and oxidative stress markers in atherosclerotic lesions is not fully established. In this study, we focused on two oxidative stress markers, dityrosine (DY) and N -(hexanoyl)lysine (HEL), which had not previously been investigated in relation to CRP in atherosclerotic lesions. Aim: We investigated the production and localization of DY, HEL, and CRP in early-stage and moderately progressed fatty lesions of cholesterol-fed rabbits by immunohistochemistry using specific monoclonal antibodies to examine the co-localization between CRP and oxidative stress in atherosclerotic lesions. Methods: Rabbit atherosclerotic specimens were obtained from New Zealand White rabbits fed a diet containing 1.0% cholesterol for 12 weeks. All specimens were fixed in formalin for histological examinations.

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The aim of the present study was to determine the effects of dietary proteins on the oxidation of dietary carbohydrate and lipids in type II diabetic mice. KK-A(y) strain mice were provided free access to a high fat diet (30% of energy as fat) for an initial 4-wk period to induce diabetes. To reduce body weight gain, the mice were subsequently fed restrictive isoenergetic and isonitrogenous diets (35% of energy as protein and 5% as fat) based on either casein or soy protein isolate hydrolysate (SPI-H) for 4 wk. To measure exogenous carbohydrate and lipid oxidation, the mice were fed a diet containing (13)C-glucose or (13)C-triolein while they were in a respiratory chamber for 72 h. Postprandial energy expenditure was higher in the SPI-H than in the casein group; this difference was due to an increase in postprandial exogenous and endogenous carbohydrate oxidation. There were no differences in 24-h energy expenditure between dietary groups. Oxidation of exogenous carbohydrate tended to be higher (P = 0.054) in the SPI-H group during the 24 h of measurement. Fecal excretion of (13)C-glucose was lower but the excretion of lipid was higher in mice fed the SPI-H diet than in casein-fed mice. These results indicate that in type II diabetic mice, dietary SPI-H not only inhibits the absorption of dietary lipids and increases the absorption of dietary carbohydrates but also augments postprandial energy expenditure, which is accompanied by a postprandial increase in oxidation of dietary carbohydrates.

To study the preventive effect of supplemented chromium picolinate (CrPic) on the development of diabetic nephropathy in mice, we analyzed the effects of CrPic supplementation on renal function and concentrations of serum glucose and tissue chromium (Cr). In experiment 1, male KK-Ay obese diabetic mice were fed either a control diet (control) or a diet supplemented with 2 mg/kg diet (Cr2) or 10 mg/kg diet (Cr10) of Cr for 12 wk. Cr10 significantly ameliorated hyperglycemia after a glucose load, creatinine clearance rates, and urinary microalbumin levels (p<0.05). In experiment 2, the Cr10 diet was fed to male KK-Ay obese diabetic mice and C57BL nondiabetic mice for 4 wk. The CrPic diet reduced urinary albumin excretion in the diabetic mice (p<0.05). Inductively coupled plasma-mass spectrometry analysis revealed that the renal Cr content and the recovery of renal Cr concentration after Cr supplementation were significantly lower in the diabetic mice than in the nondiabetic mice (p<0.01). These observations suggest that Cr supplementation of type 2 diabetic mice reduces the symptoms of hyperglycemia and improves the renal function by recovering renal Cr concentration.