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. 2021 Sep 2;162(12):bqab188. doi: 10.1210/endocr/bqab188

Figure 5.

Figure 5.

The essential role of mitochondrial oxidative-phosphorylation (OXPHOS) for fatty acid (FA)-uptake–driven adipogenesis in the hyperplastic orbital adipose tissue (OAT) expansion. Our study demonstrated a depot-specific cellular adenosine 5′-triphosphate (ATP) production via mitochondrial-OXPHOS through adipogenesis in OAT preadipocytes/fibroblasts (PFs). Dysfunction of mitochondria (dys-Mt) with disrupted OXPHOS-ATP production was observed in PFs from OAT–Graves orbitopathy (GO) due to GO factors, such as thyrotropin receptor/insulin-like growth factor 1 receptor (TSHR/IGF1R), etc (11, 17, 18, 21, 53-55). Hypothesis: Mitochondrial OXPHOS-ATP production through adipogenesis is important in maintaining OAT stability by forming a beneficial relationship with the available guanosine 5′-diphosphate (GDP) in PFs to maintain a healthy (low) level of proliferation/adipogenesis in healthy (OAT-H, highlighted in dashed blue-square). The pathological fall in OXPHOS-ATP with compensated high level of glycolysis-ATP by GO factors triggered the proliferation of PFs in OAT in GO, and kept low-level mitochondrial-OXPHOS and consequently higher GDP availability driving excessive FA-uptake–driven adipogenesis in OAT in GO (highlighted in red square). Dashed lines indicate proposed mechanism.