There is a clear correlation between obesity and the development of Type 2 Diabetes Mellitus¹. The hallmarks of Type 2 Diabetes Mellitus (T2DM) are insulin resistance, insulin insufficiency and hyperglycaemia. Normal endocrine regulation of glucose homeostasis is lost in T2DM pancreatic due to β-cell and α-cell dysfunction and eventually pancreatic β-cell loss. Obesity (BMI>30kg/m²) is caused by excess adipose lipid storage, which is associated with a significant increase in various cytokines secreted by adipose tissue including IL-1β, TNF-α and IL-6². It is known that IL-6 is a pleiotropic cytokine that is secreted by many nucleated cells including adipocytes and is linked to insulin resistance and T2DM ^3,4. The effects of pro inflammatory cytokines on nutrient metabolism in the insulin secreting pancreatic β-cell have been studied in depth⁵ in Philip Newsholmes laboratory with results indicating a change in β-cell function from insulin production to cell defense. Despite this there has been relatively little research into the effects of IL-6 or other pro-inflammatory cytokines on pancreatic α-cells. Exposure to the pleiotropic cytokine IL-6 or indeed other pro-inflammatory cytokines may result in loss of regulatory control of glucagon secretion in obese and T2DM patients. To determine the effects of IL-6 or β-cell secretory products on the functional integrity of pancreatic α-cell line, α TC1-9. α TC1-9 cells were incubated with various concentrations of glucose, glutamine and (sub lethal) combinations of IL-6, TNFα, IL-1β, IFN-γ, for various incubation times (from 0.5 to 24 hours). The cell media was analysed for glucose and glutamine to determine consumption. Cell contents were analysed for ATP, glutamate and GSH + GSSG as indicators to changes in metabolic function. Viability was determined by the WST-1 assay. Glucagon levels in the culture media were also determined. α TC1-9 cells viability and function was determined at high glucose levels (up to 25mM) and high glutamine levels (up to 5mM). No effect on cell viability in high glucose or high glutamine was determined. IL-6 at sub lethal concentrations did not alter cell viability but altered parameters of cell metabolism and glucagon secretion IL-6 alters parameters of alpha cell metabolism and function.