Daily consumption of tea containing 690 mg catechins for 12 wk reduced body fat, which suggests that the ingestion of catechins might be useful in the prevention and improvement of lifestyle-related diseases, mainly obesity.
The effects of high-fat (HF) feeding on gene expression in the small intestine were examined using obesity-resistant A/J mice and obesityprone C57BL/6J (B6) mice. Both strains of mice were maintained on low-fat (LF; 5% fat) or HF (30% fat) diets for 2 wk. Quantitative reverse transcription-PCR analysis revealed that lipid metabolism-related genes, including carnitine palmitoyltransferase (CPT) I, liver fatty acid binding protein, pyruvate dehydrogenase kinase-4, and NADP ϩ -dependent cytosolic malic enzyme, were upregulated by HF feeding in both strains of mice. The upregulated gene expression levels were higher in A/J mice than in B6 mice, suggesting more active lipid metabolism in the small intestine of A/J mice. The prominent upregulation of the lipid metabolism-related genes were specific to the small intestine; the expression levels were little or unchanged in the liver, muscle, and white adipose tissue. The increase by HF feeding and predominant expression of the intestinal lipid metabolism-related genes in A/J mice were reflected in the enzyme activities; malic enzyme, CPT, and -oxidation activities were increased by HF feeding, and the upregulated malic enzyme and CPT activities were significantly higher in obesity-resistant A/J mice compared with those in obesity-prone B6 mice. These findings suggest that intestinal lipid metabolism is associated with susceptibility to obesity. high fat; intestine; -oxidation; carnitine palmitoyltransferase; nicotinamide adenine dinucleotide phosphate ϩ -dependent cytosolic malic enzyme OBESITY IS A WELL-KNOWN RISK FACTOR for non-insulin-dependent diabetes mellitus, hypertension, and heart disease (4,14,20,29,40). Many studies (1,33,39,42) have demonstrated that obesity is a multifactorial syndrome influenced by both genetic and behavioral factors. Excessive intake of dietary fat and low levels of physical activity are representative behavioral factors. However, genetic polymorphisms in the  3 -adrenergic receptor and peroxisome proliferator-activated receptor (PPAR)-␥ gene have been reported to be associated with obesity in humans (11,37).Several studies (15,44,45,48) have also demonstrated a difference in the sensitivity to dietary fat among mouse strains; particular strains readily develop an obesity syndrome after chronic consumption of high-fat (HF) diets. C57BL/6J (B6) mice develop severe obesity accompanied by hyperglycemia when fed a HF diet. Therefore, B6 mice are among the several strains of mice classified as sensitive to diet-induced obesity. In contrast, A/J mice become only moderately obese on HF diets and are classified as resistant to diet-induced obesity.These mouse strains that differ in obesity sensitivity provide excellent experimental models to study the developmental pathophysiology of an obesity syndrome (35, 47). Watson et al. (47) have shown that leptin and uncoupling proteins were induced by the HF diet to higher levels in the adipose tissue of A/J mice compared with B6 mice, suggesting that the thermogenic capacity in adipose tissue is a ...
Lactoferrin (Lf) may play a key role in the clearance of microorganisms from a host. To study in vitro the bactericidal mechanisms of Lf during nonlactating periods, we investigated whether the effects of Lf were influenced by bovine mammary gland secretory cells (MGSC) and fresh normal bovine serum (NBS) as a source of complement. Phagocytic killing tests demonstrated that a phagocytic mixture of unopsonized Staphylococcus aureus (S. aureus) and MGSC in the presence of Lf reduced bacterial growth, compared with that of unopsonized S. aureus and MGSC without Lf. The opsonization with Lf and fresh NBS together resulted in more than a 95% reduction in CFU. The activation of complement induced by Lf also resulted in increased deposition of C3 on S. aureus, and the phagocytic activity of MGSC was augmented by opsonization with Lf and fresh NBS. Inhibition of C3 deposition by Lf was not induced in the presence of Mg‐EGTA, but was induced by the addition of bovine Lf antiserum. These results strongly suggest that Lf induces the activation of complement in fresh NBS mainly through an alternative pathway. The results demonstrated a Lf‐dependent, antibody‐independent and complement‐mediated phagocytic killing of S. aureus, and implied that Lf was synergistically capable of activating both the alternative pathway of the bovine complement cascade and phagocytosis by phagocytes.
ABSTRACT. We have identified various lactoferrin (Lf) molecules in mastitic mammary gland secretions (MGSs), and these Lf molecules were examined for their physiological function in MG. These Lf molecules were isolated by Con A affinity chromatography, and then analyzed by various electrophoresis methods and N-terminal amino acid sequencing. The low Con A affinity Lf was found to have low molecular peptides as compared with the 86 kDa of the high Con A affinity Lf, which is usually detected in healthy MGSs. The Nterminal amino acid sequence of each of the small molecular Lfs were confirmed as fragments of 86 kDa Lf. This low Con A affinity Lf stimulated spleen adherent cells to produce more O 2 -than 86 kDa Lf. Furthermore, the low Con A affinity Lf showed low antibacterial activity against E. coli and S. aureus, and had decreased iron-binding capacity in comparison with 86 kDa Lf. Moreover, the 86 kDa Lf could stimulate bovine T cells or macrophages to produce IFN-γ, IL-4, IL-6, and IL-1α. However low Con A affinity Lf induced the production of TNFα, but not physiological T cell or macrophage cytokines. It was also found that when the healthy MGs of dry cows were injected with the low Con A affinity Lf, there was an increase in polymorphonuclear cells together with TNFα, MCP-1, and IL-8 production. These results suggested that low Con A affinity Lf in mastitic MGSs differed from 86 kDa Lf in physiological characteristics, and, that it induced an inflammatory reaction in MGs. KEY WORDS: concanavalin A, lactoferrin, mammary gland secretion, mastitis.
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