{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T15:45:59Z","timestamp":1791042359027,"version":"4.1.0"},"reference-count":31,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2013,3,26]],"date-time":"2013-03-26T00:00:00Z","timestamp":1364256000000},"content-version":"vor","delay-in-days":53,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Obesity"],"published-print":{"date-parts":[[2013,2]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Objective:<\/jats:title><jats:p>Obesity is widely acknowledged as a critical risk factor for metabolic complications. Among obese subjects, there is a phenotype of metabolically healthy but obese (MHO) individuals that shows a favorable cardiometabolic risk profile. We aimed to evaluate the potential mechanisms underlying the metabolic profile of this subset, including alpha and beta cell function and entero\u2010insular axis.<\/jats:p><\/jats:sec><jats:sec><jats:title>Design and Methods:<\/jats:title><jats:p>One hundred twenty\u2010nine obese and 24 nonobese subjects were studied. Obese participants were defined as MHO or at\u2010risk obese, according to the homeostasis model of assessment\u2010insulin resistance (HOMA\u2010IR) index (MHO: lower tertile of HOMA\u2010IR, <jats:italic>n<\/jats:italic> = 43; at\u2010risk: upper tertile of HOMA\u2010IR index, <jats:italic>n<\/jats:italic> = 41). Insulin, glucagon, and incretin responses after a 120\u2032 oral glucose tolerance test (75\u2010g OGTT) were investigated.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results:<\/jats:title><jats:p>During OGTT, MHO individuals showed in comparison with at\u2010risk subjects: lower fasting and afterloads plasma levels of glucose, insulin, and C\u2010peptide; higher disposition index; lower fasting (<jats:italic>P<\/jats:italic> = 0.004) and at 30\u2032 (<jats:italic>P<\/jats:italic> = 0.01) plasma glucose\u2010dependent insulinotropic polypeptide (GIP) levels; lower area under the curve (AUC) (0\u201030) for GIP (<jats:italic>P<\/jats:italic> = 0.008); higher glucagon\u2010like peptide\u20101 (GLP\u20101) plasma levels at 90\u2032 (<jats:italic>P<\/jats:italic> = 0.02) and 120\u2032 (<jats:italic>P<\/jats:italic> = 0.02); lower glucagon plasma levels at baseline (<jats:italic>P<\/jats:italic> = 0.04) and at 30\u2032 (<jats:italic>P<\/jats:italic> = 0.03); and appropriate glucagon suppression after the oral glucose load.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions:<\/jats:title><jats:p>MHO subjects show, as well as normal\u2010weight individuals, a lower diabetogenic profile by virtue of higher disposition index and unaffected entero\u2010insular axis. At\u2010risk obese individuals present increased GIP levels that might play a role in determining increased glucagon secretion and inappropriate glucagon responses after glucose load, thus contributing to impaired glucose homeostasis.<\/jats:p><\/jats:sec>","DOI":"10.1002\/oby.20017","type":"journal-article","created":{"date-parts":[[2013,3,27]],"date-time":"2013-03-27T11:40:53Z","timestamp":1364384453000},"page":"320-325","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":32,"title":["Beta and alpha cell function in metabolically healthy but obese subjects: Relationship with entero\u2010insular axis"],"prefix":"10.1002","volume":"21","author":[{"given":"Salvatore","family":"Calanna","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Salvatore","family":"Piro","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Antonino","family":"Di 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