elastin and Weight-Gain

The aim of this study was to examine the effects of a Western diet (WD) and supplementation with Fuzhuan tea on large artery stiffness, as determined by aortic pulse wave velocity (aPWV).. Mice were subjected to a standard diet (SD; n = 12) or WD (n = 10) for 7 mo, and were then separated to receive nonsupplemented drinking water (SD-W and WD-W) or water supplemented with Fuzhuan tea (SD-T and WD-T) (200 mg/kg daily); mice were then maintained on their respective diets for an additional 2 mo.. After the initial 7-mo feeding period, WD elicited a modest and significantly greater increase in body weight than did SD (39.6 ± 0.71 versus 34.5 ± 1.16 g; P < 0.01). PWV was significantly elevated in WD but not in SD (459.3 ± 4.8 versus 422.4 ± 6.4 cm/s; P < 0.001). Following an additional 2 mo, PWV continued to increase in WD-W, but returned to control levels in WD-T (WD-W: 519.8 ± 12.8; WD-T: 426.5 ± 18.6; SD-W: 429.7 ± 8.6; SD-T: 429.1 ± 6.1 cm/s; P < 0.001, WD-W versus all groups). The increase in PWV in WD-W was accompanied by an increase in aortic collagen (WD-W: 38.8 ± 4.6 versus SD-W: 17.5 ± 5.1 percent cross-sectional area; P < 0.05).. The results of the present study suggest that the increase in arterial stiffness after modest, diet-induced weight gain can be reversed by supplementation with Fuzhuan tea.

Topics: Animals; Aorta; Camellia sinensis; Cardiovascular Agents; Collagen; Diet, Western; Dietary Supplements; Elastin; Endothelium, Vascular; Fermentation; Male; Mice, Inbred C57BL; Overweight; Plant Extracts; Plant Leaves; Pulse Wave Analysis; Random Allocation; Vascular Stiffness; Weight Gain

Apolipoprotein E knockout (apoE-KO) mice have been utilized for decades as a model of atherosclerosis. However, in addition to atherosclerosis, apoE-KO mice develop extensive cutaneous xanthomatosis, accelerated skin aging and frailty when fed a high fat diet. Granzyme B (GrB) is a pro-apoptotic serine protease that has recently been shown to exhibit extracellular proteolytic activity in certain pathologies. In the present study, the role of GrB in skin aging and pathology was assessed using the apoE-KO model of skin aging. Male C57BL/6 wild type and apoE-KO mice were grown for 0, 5, 15 or 30 weeks on either a high fat (21.2% fat, 0.2% cholesterol) or regular chow diet (7% fat). ApoE/GrB double knockout (DKO) mice were also generated and assessed after being fed either diet for 30 weeks. Skin was removed from the mid to lower back and examined for age-related changes such as hair loss, skin thinning and collagen remodeling and disorganization. ApoE-KO mice exhibited signs of frailty, hair graying, hair loss, skin thinning, loss of collagen density and increased skin pathologies featuring collagen remodeling and reduced decorin compared to wild type controls. These phenotypes occurred earlier and were more severe when fed a high fat diet. In addition, we also observed increased GrB expression in proximity to areas of decorin degradation and reduced collagen density in the skin of apoE-KO mice. DKO mice exhibited protection against skin thinning, ECM degradation and loss of dermal collagen density. In summary, our results provide novel insights into the effects of a high fat diet and apoE deficiency on skin aging and pathology and suggest a role for GrB in age-related skin thinning and frailty.

Topics: Animals; Apolipoproteins E; Collagen; Decorin; Dietary Fats; Elastin; Extracellular Matrix; Granzymes; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Models, Animal; Skin; Skin Aging; Weight Gain

Williams-Beuren syndrome (WBS) results from a deletion of 7q11.23 in 90-95% of all clinically typical cases. Clinical manifestation can be variable and therefore, deletion size, inherited elastin (ELN) and LIM kinase 1 (LIMK1) alleles, gender, and parental origin of deletion have been investigated for associations with clinical outcome. In an analysis of 85 confirmed deletion cases, no statistically significant associations were found after Bonferroni's correction for multiple pairwise comparisons. Furthermore, the present data do not support presence of imprinted genes in the WBS common deletion despite a nonsignificant excess of maternal over paternal deletions. Maternal deletion cases were more likely to have a large head circumference in the present data. Also, pairwise comparisons between individual WBS clinical features have been conducted and revealed significant associations between (1) low birth weight and poor postnatal weight gain (<10th percentile at the time of examination) and (2) transient infantile hypercalcemia and a stellate iris pattern. The latter association could indicate a common underlying etiology.

Topics: Alleles; Birth Weight; Chromosomes, Human, Pair 7; Elastin; Female; Gene Frequency; Genomic Imprinting; Genotype; Humans; Hypercalcemia; Infant, Newborn; Lim Kinases; Linkage Disequilibrium; Male; Phenotype; Polymorphism, Genetic; Protein Kinases; Sequence Deletion; Weight Gain; Williams Syndrome

To evaluate the effects of exercise on aortic wall elasticity and elastic components, young male rats underwent various exercise regimes for 16 weeks. In the exercised rats, the aortic incremental elastic modulus decreased significantly when under physiological strain. The aortic content of elastin increased significantly and the calcium content of elastin decreased significantly in the exercised group. The accumulated data from the exercised and sedentary groups revealed that the elastin calcium content was related positively to the incremental elastic modulus. We concluded that physical exercise from an early age decreases the calcium deposit in aortic wall elastin and that this effect probably produced in the exercised rats a distensible aorta.

Topics: Animals; Aorta; Calcium; Collagen; Elastic Tissue; Elasticity; Elastin; Male; Muscle, Smooth, Vascular; Physical Conditioning, Animal; Rats; Rats, Inbred WKY; Tensile Strength; Weight Gain

Prolonged hyperoxic exposure is associated with impaired alveolarization of the lung in both the rat and the human neonate. Elastin is currently thought to play a pivotal role in the alveolarization of the lung by providing the structural framework around which new alveoli will develop. Previous studies in both the rat and the human neonate have demonstrated a risk for proteolytic destruction of lung elastin associated with prolonged hyperoxic exposure. The present study was undertaken to determine whether continuous exposure to 100% oxygen during the period of alveolar development in the rat (Days 4 to 13) would alter lung elastin. Parenchymal lung elastic fiber length, volume density of parenchyma, mean linear intercept, and internal surface area were quantitated using morphometric techniques, and the values were compared in control, oxygen-exposed, and malnourished rat pups. Stereologic measurements indicated that total elastic fiber length was significantly greater in lungs of control pups than in lungs of either the oxygen-exposed or the malnourished pups. Examination of sections of lung tissue 20 to 30 microns thick indicated altered elastic fiber structure and numerous alveolar fenestrae only in the hyperoxic pups. The results of these studies demonstrated that hyperoxic exposure during alveolarization alters both total length and structure of lung elastic fibers and suggest that impaired lung development might be due in part to these observed changes.

Topics: Animals; Animals, Newborn; Elastic Tissue; Elastin; Female; Histological Techniques; Lung; Male; Nutrition Disorders; Oxygen; Pulmonary Alveoli; Rats; Rats, Inbred Strains; Weight Gain