Hypoadiponectinemia in lipoatrophy may be related to worsening of hypertension in stroke-prone spontaneously hypertensive rats (SHRSP). One of the beneficial effects of candesartan (Angiotensin II Type 1 receptor blocker) for preventing hypertension may be increasing of adiponectin due to improvement of adipocyte dysfunction. In this study, we determined the effects of candesartan or adiponectin on pathophysiologic features and adipocyte dysfunction in SHRSP. Candesartan was administered to male SHRSP from 16 to 20 weeks of age (2 mg/kg/day). Adiponectin was cloned and intravenously administered to male SHRSP from 16 to 20 weeks of age. We examined biological parameters, as well as the expression and release of adipokines. The SHRSP exhibited severe atrophy of visceral fat and progression of severe hypertension. The expression and release of leptin and adiponectin were impaired at 6 and 20 weeks of age. Candesartan suppressed the development of lipoatrophy and reduced the incidence of stroke at 20 weeks of age. Candesartan also enhanced the expression of adiponectin and leptin by inducing the overexpression of peroxisome proliferator activated receptor γ. Circulating level of leptin was significantly higher in candesartan group than in the control group, whereas adiponectin was similar in both groups. Intravenous administration of adiponectin resulted in enhancement of adiponectin expression in adipose tissue, but no remarkable effects were found in pathophysiology in SHRSP. Our results indicate that candesartan protects against hypertension and adipocyte dysfunction in SHRSP. The induction of leptin expression appeared to be important factor in the inhibition of stroke lesions, whereas adiponectin was not a major regulator of blood pressure in SHRSP with genetic hypertension. Further studies are needed to elucidate the role of the renin–angiotensin system in adipose tissue dysfunction in relation to hypertensive end-organ damage.

Skin aging is intrinsic and extrinsic. Intrinsic, or chronological, skin aging is an inevitable process of chronological and physiological alterations. The factors contributing to extrinsic skin aging involve sunlight, nutrients, and stress. Thus, extrinsic aging is thought to be superimposed over intrinsic aging and depends on the intensity and duration of environmental exposure and skin type (e.g., dry skin, oily skin, or eczema). The most significant extrinsic aging factor is UV radiation, which causes cellular senescence in a process known as photoaging. This study aimed to illuminate the mechanism whereby solubilized elastin peptide lotion (EL) from the bulbus arteriosus of yellowtail (Seriola quinqueradiata) prevents skin photoaging in hairless mice. EL reduced wrinkle formation, epidermal skin thickness, and Ki67 (cell growth marker) mRNA expression in skin tissues from ultraviolet B (UVB)-irradiated mice. EL treatment also reduced glyoxalase-1 (key enzyme of glucose metabolism) levels in skin tissue. Although no significant differences in collagen and elastin contents were found in dermal areas, matrix metalloproteinase-12 (wrinkle-related marker) expression was reduced following EL application. Furthermore, skin DPP-IV/CD26 (new senescence marker) levels decreased following EL treatment in photoaging model mice. These results suggest that EL moderates skin damage caused by UVB irradiation by regulating senescence-related molecule expression.