Yes. Elevated blood sugar accelerates a process called glycation — where glucose molecules attach non-enzymatically to proteins like collagen, cross-linking them and reducing skin elasticity over time.
The chemistry is well-established. Monnier's foundational 1990 paper described the Maillard reaction as a driver of aging — the same reaction that browns crust on bread is happening slowly to your collagen when circulating glucose is chronically elevated (Monnier, 1990). The end products, called advanced glycation end products (AGEs), stiffen collagen and reduce its ability to remodel.
Skin collagen has a slow turnover — roughly a fifteen-year half-life for dermal collagen (Verzijl et al., 2000) — which is why glycation damage accumulates. Whatever elevation of glucose you carry today shows up years from now as skin that has lost elasticity and looks structurally older.
The best measurable proxy is HbA1c, which reflects your average blood sugar over the last three months. Clinically, an HbA1c of 5.9 is called normal. For skin, values that live in the high end of clinical normal are already producing measurable glycation — Selvin and colleagues showed elevated glycation risk begins well below the pre-diabetic threshold (Selvin, 2010).
Fasting glucose gives you today's snapshot. Fasting insulin often shifts earlier than either. The three markers together tell you where you sit metabolically, and whether the glycation load on your skin is high, moderate, or well controlled.
All three are on the JenSkin panel for exactly this reason.