Consistent with the mitochondrial responses, extended hyperglycemia may disrupt the physiological crosstalk between INS‐1 and adipocytes with increased TNF‐α, IL‐6, and insulin levels, leading to aggravated inflammatory state and beta cell stress with excess calcium influx and insulin production.[51] As beta cell function diminishes, insulin secretion becomes insufficient to counteract insulin resistance, leading to impaired glucose tolerance and eventually the onset of diabetes.[52, 53] In our monocultures, IL‐6 incubation increased insulin secretion from INS‐1 cells. Here, INS is linked to Impaired glucose tolerance.