Effects of green tea on growth, food utilization and lipid metabolism in mice.

To find whether green tea has anti-obesity effects in mice, female ICR mice were fed on diets containing 1, 2 and 4% green tea powder for 16 weeks and the body weight and food intake were weighed. After the administration of green tea, the ovaries, kidneys, adrenals, liver, spleen, brain, pituitary and intraperitoneal adipose tissues in the mice were weighed and lipid levels in the serum and in the liver and serum leptin levels were measured. It was found that body weight increase and intraperitoneal adipose tissues were remarkably suppressed by the administration of diets containing 2 and 4% green tea powder. Food intake was suppressed by feeding the 4% green tea diet. Concentrations of total cholesterol in the liver, triglycerides in serum and liver and nonestrified fatty acids in serum from mice which were administered green tea diet were lower than those in the controls. Leptin levels in serum showed a decrease with green tea treatments. These results indicated that lipid metabolism in mice was suppressed by the administration of green tea powder and thereby the fatty accumulation and body weight increase was suppressed.

Different effects of dominant negative mutants of desmocollin and desmoglein on the cell-cell adhesion of keratinocytes.

Desmosomes contain two types of cadherin: desmocollin (Dsc) and desmoglein (Dsg). In this study, we examined the different roles that Dsc and Dsg play in the formation of desmosomes, by using dominant-negative mutants. We constructed recombinant adenoviruses (Ad) containing truncated mutants of E-cadherin, desmocollin 3a, and desmoglein 3 lacking a large part of their extracellular domains (EcaddeltaEC, Dsc3adeltaEC, Dsg3deltaEC), using the Cre-loxP Ad system to circumvent the problem of the toxicity of the mutants to virus-producing cells. When Dsc3adeltaEC Ad-infected HaCaT cells were cultured with high levels of calcium, E-cadherin and beta-catenin, which are marker molecules for the adherens junction, disappeared from the cell-cell contact sites, and cell-cell adhesion was disrupted. This also occurred in the cells infected with EcaddeltaEC Ad. With Dsg3deltaEC Ad infection, keratin insertion at the cell-cell contact sites was inhibited and desmoplakin, a marker of desmosomes, was stained in perinuclear dots while the adherens junctions remained intact. Dsc3adeltaEC Ad inhibited the induction of adherens junctions and the subsequent formation of desmosomes with the calcium shift, while Dsg3deltaEC Ad only inhibited the formation of desmosomes. To further determine whether Dsc3adeltaEC directly affected adherens junctions, mouse fibroblast L cells transfected with E-cadherin (LEC5) were infected with these mutant Ads. Both Dsc3adeltaEC and EcaddeltaEC inhibited the cell-cell adhesion of LEC5 cells, as determined by the cell aggregation assay, while Dsg3deltaEC did not. These results indicate that the dominant negative effects of Dsg3deltaEC were restricted to desmosomes, while those of Dsc3adeltaEC were observed in both desmosomes and adherens junctions. Furthermore, the cytoplasmic domain of Dsc3adeltaEC coprecipitated both plakoglobin and beta-catenin in HaCaT cells. In addition, beta-catenin was found to bind the endogenous Dsc in HaCaT cells. These findings lead us to speculate that Dsc interacts with components of the adherens junctions through beta-catenin, and plays a role in nucleating desmosomes after the adherens junctions have been established.

Effects of green tea and tea catechins on the development of mammary gland.

To find whether green tea and tea catechins have effects on the development of mammary glands, virgin DDD mice were fed on diets containing green tea and tea catechins. The degree of mammary gland development was examined by duct-alveolar growth and DNA content. The results indicated that green tea, but not tea catechins, has a growth-promoting effect on mammary gland development.

High-dose tocopherol acetate therapy in epidermolysis bullosa siblings of the Cockayne-Touraine type.

We have employed a successful therapy for epidermolysis bullosa with high-dose oral tocopherol acetate. Two siblings with dominant dystrophic epidermolysis bullosa of the Cockayne-Touraine type were reported. Both siblings suffered from tense blisters and erosions healing with scars and transient milia on the extremities. Electron microscopic study of the blisters revealed a cleavage beneath the lamina densa in both siblings. High-dose oral tocopherol acetate therapy was administered to them with satisfactory clinical reduction of the blister formation.