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In prenatal caloric-restricted rats with intrauterine growth restriction (IUGR) and postnatal exposure to high fat with fructose (HFhf) or high carbohydrate, we investigated male and female IUGR-HFhf and IUGR-high carbohydrate, vs HFhf and control offspring. Males more than females displayed adiposity, glucose intolerance, insulin resistance, hyperlipidemia, and hepatomegaly with hepatic steatosis. Male hepatic triglyceride synthesis, de novo lipogenesis genes increased, while female lipolysis, \u03b2-oxidation, fatty acid efflux, and FGF21 genes increased. IUGR-HFhf males demonstrated reduced \u03b2-islet insulin and humanin, and type 1 diabetes mellitus human amniotic fluid increased humanin. Humanin suppression disabled glucose stimulated insulin, ATP production, with apoptotic diminished \u03b2-islet viability. Humanin and FGF21 may reverse perinatal nutritional mismatched phenotype by restoring functional \u03b2 islets and preventing metabolic dysfunction-associated steatotic liver disease and diabetes mellitus.<\/jats:p>","DOI":"10.1210\/endocr\/bqaf007","type":"journal-article","created":{"date-parts":[[2025,1,17]],"date-time":"2025-01-17T19:59:19Z","timestamp":1737143959000},"source":"Crossref","is-referenced-by-count":2,"title":["Hepatic and Pancreatic Cellular Response to Early Life Nutritional Mismatch"],"prefix":"10.1210","volume":"166","author":[{"given":"Shubhamoy","family":"Ghosh","sequence":"first","affiliation":[{"name":"Division of Neonatology & Developmental Biology, Department of Pediatrics, UCLA Children\u2019s Discovery & Innovation Institute at the David Geffen School of Medicine at UCLA , Los Angeles, CA 90095-1752 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