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Objective  Obesity and type 2 diabetes mellitus are risk factors for developing Alzheimer disease. Overlapping patterns of metabolic dysfunction may be common molecular links between these complex diseases. Amyloid‐β (Aβ) precursor protein and associated β‐ and γ‐secretases are expressed in adipose tissue. Aβ precursor protein is up‐regulated with obesity and correlated to insulin resistance. Aβ may be secreted by adipose tissue, its production may be regulated through metabolic pathways, and Aβ may exert effects on adipose tissue insulin receptor signaling.    Methods  Human stromal‐vascular cells and differentiated adipocytes were cultured with different combinations of glucose and insulin and then assayed for Aβ in conditioned media. Aβ was measured  in vivo  using adipose tissue microdialysis.    Results  Aβ secretion was increased by glucose and insulin  in vitro . Adipose tissue microdialysates contained Aβ. Adipocytes treated with Aβ had decreased expression of insulin receptor substrate‐2 and reduced Akt‐1 phosphorylation.    Conclusions  Aβ was made by adipose tissue cells  in vitro  at concentrations similar to  in vivo  measurements. Regulation of Aβ production by glucose and insulin and effects of Aβ on the insulin receptor pathway suggest similar cellular mechanisms may exist between neuronal dysfunction in Alzheimer disease and adipose dysfunction in type 2 diabetes.

Effects of glucose and insulin on secretion of amyloid‐β by human adipose tissue cells