Purpose: Metabolic diseases share common risk factors, requiring the development of therapeutic agents with multi-target effects. Although the ameliorating effects of Porphyra tenera ethanol extract (PTE) have been reported on some individual metabolic disorders, studies addressing various other metabolic diseases are still limited. This study investigated the ameliorating effects of PTE supplementation for 12 weeks on obesity, dyslipidemia, and hepatic lipid metabolism in high-fat diet (HFD)-induced obese mice and its molecular mechanisms. Methods: Male C57BL/6 mice (n = 12/in each group) were divided into six groups for 12 weeks: control, HFD, chow diet + 1% porphyran, chow diet + 4% porphyran, HFD + 1% porphyran (HPYP-L), and HFD + 4% porphyran (HPYP-H). To confirm the attenuation of metabolic disease in vivo, mice in the HFD, HPYP-L and HPYP-H groups were fed 60% HFD to induce obesity. PTE was prepared using ethanol and dissolved in drinking water to concentrations of 1% and 4% porphyran. After 12 weeks of free PTE intake, body weight measurement, serum analysis, histopathological analysis, real-time quantitative polymerase chain reaction, and Western blot analysis of liver tissues were performed for comparative evaluation. Results: After 12 weeks, the HPYP-L and HPYP-H groups showed a decreased body weight, improved blood lipids, and reduced hepatic lipid droplet accumulation vs. the HFD group.Liver acetyl-CoA carboxylase, was suppressed in the HPYP-L group vs. the HFD group.The B-cell lymphoma 2 (Bcl-2)-associated X protein/Bcl-2 protein and messenger RNA (mRNA) level ratio in the liver decreased after PTE intake, indicating inhibition of apoptosis.Interleukin-1 beta mRNA expression in the liver was reduced in the HPYP-L group vs. the HFD group. In the liver, lower protein carbonylation levels in the HPYP-H group indicated reduced oxidative stress, while the increased mitochondrial DNAuclear DNA ratio indicated improved mitochondrial function. Conclusion PTE protects against diet-induced metabolic disorders and could be a potential agent for the prevention and treatment of metabolic diseases.

Purpose: Metabolic diseases share common risk factors, requiring the development of therapeutic agents with multi-target effects. Although the ameliorating effects of Porphyra tenera ethanol extract (PTE) have been reported on some individual metabolic disorders, studies addressing various other metabolic diseases are still limited. This study investigated the ameliorating effects of PTE supplementation for 12 weeks on obesity, dyslipidemia, and hepatic lipid metabolism in high-fat diet (HFD)-induced obese mice and its molecular mechanisms. Methods: Male C57BL/6 mice (n = 12/in each group) were divided into six groups for 12 weeks: control, HFD, chow diet + 1% porphyran, chow diet + 4% porphyran, HFD + 1% porphyran (HPYP-L), and HFD + 4% porphyran (HPYP-H). To confirm the attenuation of metabolic disease in vivo, mice in the HFD, HPYP-L and HPYP-H groups were fed 60% HFD to induce obesity. PTE was prepared using ethanol and dissolved in drinking water to concentrations of 1% and 4% porphyran. After 12 weeks of free PTE intake, body weight measurement, serum analysis, histopathological analysis, real-time quantitative polymerase chain reaction, and Western blot analysis of liver tissues were performed for comparative evaluation. Results: After 12 weeks, the HPYP-L and HPYP-H groups showed a decreased body weight, improved blood lipids, and reduced hepatic lipid droplet accumulation vs. the HFD group.Liver acetyl-CoA carboxylase, was suppressed in the HPYP-L group vs. the HFD group.The B-cell lymphoma 2 (Bcl-2)-associated X protein/Bcl-2 protein and messenger RNA (mRNA) level ratio in the liver decreased after PTE intake, indicating inhibition of apoptosis.Interleukin-1 beta mRNA expression in the liver was reduced in the HPYP-L group vs. the HFD group. In the liver, lower protein carbonylation levels in the HPYP-H group indicated reduced oxidative stress, while the increased mitochondrial DNAuclear DNA ratio indicated improved mitochondrial function. Conclusion PTE protects against diet-induced metabolic disorders and could be a potential agent for the prevention and treatment of metabolic diseases.

Purpose: Metabolic diseases share common risk factors, requiring the development of therapeutic agents with multi-target effects. Although the ameliorating effects of Porphyra tenera ethanol extract (PTE) have been reported on some individual metabolic disorders, studies addressing various other metabolic diseases are still limited. This study investigated the ameliorating effects of PTE supplementation for 12 weeks on obesity, dyslipidemia, and hepatic lipid metabolism in high-fat diet (HFD)-induced obese mice and its molecular mechanisms. Methods: Male C57BL/6 mice (n = 12/in each group) were divided into six groups for 12 weeks: control, HFD, chow diet + 1% porphyran, chow diet + 4% porphyran, HFD + 1% porphyran (HPYP-L), and HFD + 4% porphyran (HPYP-H). To confirm the attenuation of metabolic disease in vivo, mice in the HFD, HPYP-L and HPYP-H groups were fed 60% HFD to induce obesity. PTE was prepared using ethanol and dissolved in drinking water to concentrations of 1% and 4% porphyran. After 12 weeks of free PTE intake, body weight measurement, serum analysis, histopathological analysis, real-time quantitative polymerase chain reaction, and Western blot analysis of liver tissues were performed for comparative evaluation. Results: After 12 weeks, the HPYP-L and HPYP-H groups showed a decreased body weight, improved blood lipids, and reduced hepatic lipid droplet accumulation vs. the HFD group.Liver acetyl-CoA carboxylase, was suppressed in the HPYP-L group vs. the HFD group.The B-cell lymphoma 2 (Bcl-2)-associated X protein/Bcl-2 protein and messenger RNA (mRNA) level ratio in the liver decreased after PTE intake, indicating inhibition of apoptosis.Interleukin-1 beta mRNA expression in the liver was reduced in the HPYP-L group vs. the HFD group. In the liver, lower protein carbonylation levels in the HPYP-H group indicated reduced oxidative stress, while the increased mitochondrial DNAuclear DNA ratio indicated improved mitochondrial function. Conclusion PTE protects against diet-induced metabolic disorders and could be a potential agent for the prevention and treatment of metabolic diseases.