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We show that palmitoylation cycling in white adipose tissue (WAT) balances insulin sensitivity and insulin secretion. WAT and brown adipose tissue (BAT) ablation of acyl-protein thioesterase 1 (APT1) in APT1-deficient (knockout) mice (APT1-AdipoKO) resulted in increased body weight and exacerbated insulin resistance when the mice were fed a high-fat diet (HFD). APT1 ablation limited to BAT decreased body weight without affecting insulin resistance or glucose metabolism in HFD-fed mice. Insulin-stimulated Akt phosphorylation was decreased in gonadal WAT, muscle, and liver of APT1-AdipoKO mice and in APT1 knockdown 3T3-L1 adipocytes. APT1-deficient gonadal WAT adipocytes were enlarged and had increased isoproterenol-stimulated lipolysis compared with control adipocytes. Despite greater insulin resistance, HFD-fed APT1-AdipoKO mice had normal glucose tolerance, preserved \u03b2-cell mass, and increased cell-autonomous glucose-stimulated insulin secretion (GSIS). Chow-fed APT1-AdipoKO mice at age 12\u201314 months had insulin resistance with improved glucose tolerance, increased \u03b2-cell mass, and increased cell-autonomous GSIS. Extracellular vesicles prepared from APT1-deficient 3T3-L1 adipocytes increased GSIS in INS-1 cells. These results suggest the palmitoylation status of visceral adipose tissue can protect against glucose intolerance in the setting of sustained insulin resistance in mice by preserving \u03b2-cell function.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title\/>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Article Highlights<\/jats:title>\n                    <jats:p>Palmitoylation, the reversible modification of proteins by palmitate, is altered in diabetes. We inactivated acyl protein thioesterase-1 (APT1), a key palmitoylation cycling enzyme, in adipose tissue to study how fat affects systemic metabolism. Given adiposity effects on \u03b2-cell failure, we asked if palmitoylation of proteins in fat affects insulin secretion. Adipose APT1-deficient mice had improved glucose metabolism and increased cell-autonomous insulin secretion in two models of insulin resistance, high-fat diet, and aging. Extracellular vesicles from APT1-deficient adipocytes promoted insulin secretion in insulinoma cells. Altering palmitoylation in fat may preserve \u03b2-cell function in insulin resistance.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.2337\/db26-0023","type":"journal-article","created":{"date-parts":[[2026,8,3]],"date-time":"2026-08-03T19:47:56Z","timestamp":1785786476000},"page":"1767-1780","update-policy":"https:\/\/doi.org\/10.2337\/ada-journal-policies","source":"Crossref","is-referenced-by-count":0,"title":["Adipose Tissue Palmitoylation Cycling Mediates Insulin Resistance and Preservation of \u03b2-Cell Function in Mice"],"prefix":"10.2337","volume":"75","author":[{"given":"Guifang","family":"Dong","sequence":"first","affiliation":[{"name":"Division of Endocrinology, Metabolism & Lipid Research, Washington University 1 , St. Louis, MO"},{"name":"Hubei Key Laboratory of Animal Nutrition and Feed Science, Wuhan Polytechnic University 2 , Wuhan, 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