https://orcid.org/0000-0003-4395-5248
Figures & data
Figure 1 The regulation mechanism of luteinizing hormone (LH) and growth hormone (GH) on glucose homeostasis. LH indirectly affects glucose homeostasis by interfering with related signaling pathways through androgens and inflammatory mediators, while GH interferes with insulin signaling through p85α.
Abbreviations: IRS-1, insulin receptor substrate-1; PI3K, phosphoinositide 3-kinase; GLUT4, glucose transporter 4; AR, androgen receptor; JAK2, Janus tyrosine kinase 2; STAT3, signal transducers and activators of transcription 3; PPAR-γ, peroxisome proliferator activated receptor γ; IL-6, interleukin 6.
Figure 2 Excessive GCs act on the above-mentioned organs to induce glucose metabolism disorders and eventually lead to hyperglycemia.
Abbreviations: IRS, insulin receptor substrate; PI3K, phosphoinositide 3-kinase; MKP-3, mitogen-activated protein kinase phosphatase-3; FOXO1, forkhead box protein O1; AA, amino acid; FFA, free fatty acids; NEFAs, non-esterified fatty acids; ATGL, adipose triglyceride lipase; NPY, nerve peptide Y; AgRP, agouti-related protein; JAK, Janus tyrosine kinase; STAT, signal transducers and activators of transcription.
Figure 3 The regulatory mechanism of thyroid stimulating hormone (TSH) on glucose metabolism. TSH induces gluconeogenesis and insulin resistance through the TSHR/cAMP/PKA pathway.
Abbreviations: CRTC2, cAMP-regulated transcriptional coactivators 2; cAMP, cyclic adenosine monophosphate; CREB, cAMP-response element binding protein; PEPCK, phosphoenolpyruvate carboxykinase; G6P, glucose-6-phosphatase; PKA, protein kinase A; TSHR, thyroid stimulating hormone receptor; IRS-1, insulin receptor substrate 1; PI3K, phosphoinositide 3-kinase.
Figure 4 Relationship between the melanocortin system and diabetes.
Abbreviation: POMC, proopiomelanocortin.
