{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T06:04:38Z","timestamp":1789970678484,"version":"4.0.1"},"reference-count":40,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Endocrinology and Metabolism"],"published-print":{"date-parts":[[2012,1,1]]},"abstract":"<jats:p> Low birth weight (LBW) is associated with an increased risk of insulin resistance and downregulation of oxidative phosphorylation (OXPHOS) genes when exposed to a metabolic challenge of high-fat overfeeding (HFO). To elaborate further on the differential effects of HFO in LBW subjects, we measured in vivo mitochondrial function, insulin secretion, hepatic glucose production, and plasma levels of key regulatory hormones before and after 5 days of HFO in 20 young LBW and 26 normal-birth-weight (NBW) men. The LBW subjects developed peripheral insulin resistance after HFO due to impaired endogenous glucose storage (9.42 \u00b1 4.19 vs. 5.91 \u00b1 4.42 mg\u00b7kg FFM<jats:sup>\u22121<\/jats:sup>\u00b7min<jats:sup>\u22121<\/jats:sup>, P = 0.01). Resting muscle phosphorcreatine and total ATP in muscle increased significantly after HFO in LBW subjects only, whereas additional measurements of mitochondrial function remained unaffected. Despite similar plasma FFA levels, LBW subjects displayed increased fat oxidation during insulin infusion compared with normal-birth-weight (NBW) subjects after HFO (0.37 \u00b1 0.35 vs. 0.17 \u00b1 0.33 mg\u00b7kg FFM<jats:sup>\u22121<\/jats:sup>\u00b7min<jats:sup>\u22121<\/jats:sup>, P = 0.02). In contrast to NBW subjects, the plasma leptin levels of LBW subjects did not increase, and the plasma gastric inhibitory polypeptide (GIP) as well as pancreatic polypeptide (PP) levels increased less in LBW compared with NBW subjects during HFO. In conclusion, HFO unmasks dissociation between insulin resistance and mitochondrial dysfunction in LBW subjects, suggesting that insulin resistance may be a cause, rather than an effect, of impaired muscle OXPHOS gene expression and mitochondrial dysfunction. Reduced increments in response to HFO of fasting plasma leptin, PP, and GIP levels may contribute to insulin resistance, lower satiety, and impaired insulin secretion in LBW subjects. <\/jats:p>","DOI":"10.1152\/ajpendo.00095.2011","type":"journal-article","created":{"date-parts":[[2011,9,14]],"date-time":"2011-09-14T06:56:16Z","timestamp":1315983376000},"page":"E43-E51","source":"Crossref","is-referenced-by-count":48,"title":["Effects of high-fat overfeeding on mitochondrial function, glucose and fat metabolism, and adipokine levels in low-birth-weight subjects"],"prefix":"10.1152","volume":"302","author":[{"given":"Charlotte","family":"Br\u00f8ns","sequence":"first","affiliation":[{"name":"Steno Diabetes Center, Gentofte, Denmark;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stine","family":"Jacobsen","sequence":"additional","affiliation":[{"name":"Steno Diabetes Center, Gentofte, Denmark;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Natalie","family":"Hiscock","sequence":"additional","affiliation":[{"name":"Unilever Discover Research and Development, Colworth Science Park, Sharnbrook, Bedfordshire;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrew","family":"White","sequence":"additional","affiliation":[{"name":"Unilever Discover Research and Development, Colworth Science Park, Sharnbrook, Bedfordshire;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Emma","family":"Nilsson","sequence":"additional","affiliation":[{"name":"Steno Diabetes Center, Gentofte, Denmark;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David","family":"Dunger","sequence":"additional","affiliation":[{"name":"Department of Paediatrics, University of Cambridge, Addenbrooke's Hospital, Cambridge, United Kingdom;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Arne","family":"Astrup","sequence":"additional","affiliation":[{"name":"Department of Human Nutrition, The Faculty of Life Sciences; 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