Research press release





今回、Matthew Vander Heiden、Brian Wolpinたちの研究グループは、膵臓がんのマウスモデルを用いて、脂肪組織と骨格筋の重量が、がんの発生初期に減少することを明らかにした。こうした末梢組織の消耗は、膵臓で腫瘍が増殖した場合だけ起こり、その他の臓器の場合には起こらないことも判明した。さらに研究グループは、膵臓の外分泌機能の低下によって脂肪細胞の減少が引き起こされており、膵酵素の補充によって末梢組織の消耗は減衰するが、マウスの生存率は改善しないことを明らかにした。


Altered exocrine function in the pancreas may be responsible for the wasting of adipose tissue and skeletal muscle experienced by patients with pancreatic cancer, suggests a study published this week in Nature.

Changes in cellular metabolism are symptoms of various forms of cancers. Pancreatic cancer is especially associated with the wasting of peripheral tissues, a metabolic syndrome that lowers quality of life and is thought to decrease survival of patients with cancer. Tissue wasting is a condition with many contributing factors, but pinpointing the exact underlying mechanisms has been difficult.

Using mouse models of pancreatic cancer, Matthew Vander Heiden, Brian Wolpin and colleagues find that adipose tissue and skeletal muscle loss occurs early in the development of the disease. They find that tumour growth in the pancreas, but not in other areas, leads to the wasting of peripheral tissues. The authors also show that decreased exocrine pancreatic function drives adipose tissue loss, and that supplementing pancreatic enzymes attenuates peripheral tissue wasting, but does not improve survival of mice.

In a cohort of 782 patients with pancreatic cancer, 65% had evidence of skeletal muscle wasting at diagnosis. However, adipose tissue and skeletal muscle wasting were not associated with reduced survival in patients. Thus, peripheral tissue wasting that occurs in the setting of early pancreatic cancer may serve as an early warning sign of the disease, but was not necessarily linked to shorter survival.

doi: 10.1038/s41586-018-0235-7

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