Insulin is a small peptide hormone synthesized and secreted by pancreatic beta cells; human insulin is produced from proinsulin by enzymatic cleavage and is 51 amino acids long. It belongs to the class of peptide hormones that signal through surface receptors to change cellular transport and metabolic enzyme activity. The hormone was identified and characterized in the early 20th century, establishing its central role in blood sugar regulation and prompting the development of laboratory assays to measure circulating levels. Biologically, insulin promotes glucose uptake into muscle and fat cells, stimulates glycogen and lipid synthesis, and suppresses glucose production and fat breakdown in the liver. It also influences protein synthesis and has indirect effects on blood vessels and inflammatory pathways through its metabolic actions. Because insulin reflects both pancreatic secretion and tissue response, it functions as a core marker for assessing metabolic load and signaling dynamics in clinical testing.

Elevated fasting insulin often reflects a compensatory increase in secretion when tissues are less responsive to insulin, recent carbohydrate intake, or slower hormone clearance; in population studies, higher insulin levels commonly track with altered lipid patterns, inflammation markers, and greater metabolic strain. Low insulin levels can occur with prolonged fasting, reduced pancreatic secretion, or when cells are highly insulin-sensitive; low levels may coincide with low circulating glucose or differences in hormone production and clearance. Interpretation requires the full clinical and laboratory context: compare insulin with fasting glucose, HbA1c, C‑peptide, HOMA-IR, lipid and inflammatory markers, and clinical history to understand whether patterns reflect acute changes, chronic metabolic adaptation, or measurement timing.

Insulin is included in Cardio Zoomer to characterize metabolic response and glycemic load as part of a systems-level cardiovascular assessment. It helps distinguish whether metabolic strain or altered insulin signaling is contributing to adverse lipid profiles, inflammation, or endothelial stress, informing personalized risk patterns and targeted follow-up testing.