인문학
사회과학
자연과학
공학
의약학
농수해양학
예술체육학
복합학
지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
커뮤니티
연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
초록·키워드
Sphingolipids are evolutionarily conserved lipids that, I contend, emerged as a solution to a fundamental biochemical problem: cells require fatty acids, yet these molecules are potent detergents. In higher metazoans, a metabolic asymmetry amplifies this physical threat: unlike most macronutrients, fatty acids cannot be readily converted into nonlipid forms of biomass. Thus, when their supply exceeds energetic demand, they remain chemically committed lipids with the capacity to destabilize membranes and disrupt cellular organization. The emergence of sphingolipid metabolism offered an elegant solution to this challenge. By incorporating fatty acids into sphingolipids, cells both stabilize membranes to combat detergent stress and generate ceramide-dependent signaling programs that coordinate metabolic adaptation, remodeling, and, when necessary, cell elimination in response to lipid overload. In modern settings of chronic lipid surplus, most prominently obesity, this otherwise adaptive system becomes pathological. Across liver, adipose tissue, skeletal muscle, heart, pancreas, and kidney, excessive sphingolipid accumulation enforces metabolic inflexibility, impairs mitochondrial efficiency, and promotes cell dysfunction or loss, contributing to diabetes, steatohepatitis, heart failure, and kidney disease. Human studies consistently associate circulating ceramide species with cardiometabolic risk, while interventional studies in rodents demonstrate their causal roles in disease progression. Together, these findings position sphingolipids-much like cholesterol-as both early biomarkers and modifiable drivers of chronic disease, highlighting how an evolutionary solution becomes pathogenic in the setting of prolonged nutrient excess.
인공지능 문자 인식 모델을 통해 추출된 텍스트로, 일부 오타나 오류가 포함될 수 있으나 지속적으로 개선 중입니다.
오류를 발견하셨다면 해당 부분을 드래그한 후 ' 를 통해 신고해주세요.
오류를 발견하셨다면 해당 부분을 드래그한 후 ' 를 통해 신고해주세요.