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L E Nicol Pediatrics, Division of Neurosciences, Pape Pediatric Research Institute

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W R Grant Pediatrics, Division of Neurosciences, Pape Pediatric Research Institute

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S M Comstock Pediatrics, Division of Neurosciences, Pape Pediatric Research Institute

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M L Nguyen Pediatrics, Division of Neurosciences, Pape Pediatric Research Institute

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M S Smith Pediatrics, Division of Neurosciences, Pape Pediatric Research Institute

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K L Grove Pediatrics, Division of Neurosciences, Pape Pediatric Research Institute

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D L Marks Pediatrics, Division of Neurosciences, Pape Pediatric Research Institute
Pediatrics, Division of Neurosciences, Pape Pediatric Research Institute

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L E Nicol Pediatrics, Division of Neurosciences, Pape Pediatric Research Institute

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W F Grant Pediatrics, Division of Neurosciences, Pape Pediatric Research Institute

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S M Comstock Pediatrics, Division of Neurosciences, Pape Pediatric Research Institute

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M L Nguyen Pediatrics, Division of Neurosciences, Pape Pediatric Research Institute

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M S Smith Pediatrics, Division of Neurosciences, Pape Pediatric Research Institute

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K L Grove Pediatrics, Division of Neurosciences, Pape Pediatric Research Institute

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D L Marks Pediatrics, Division of Neurosciences, Pape Pediatric Research Institute
Pediatrics, Division of Neurosciences, Pape Pediatric Research Institute

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Chronic high caloric intake has contributed to the increased prevalence of pediatric obesity and related morbidities. Most overweight or obese children, however, do not present with frank metabolic disease but rather insulin resistance or subclinical precursors. The innate immune system plays a role in the pathophysiology of type 2 diabetes but how it contributes to early metabolic dysfunction in children on chronic high-fat diet (HFD) is unclear. We hypothesize that such inflammation is present in the pancreas of children and is associated with early insulin resistance. We used nonhuman primate (NHP) juveniles exposed to chronic HFD as a model of early pediatric metabolic disease to demonstrate increased pancreatic inflammatory markers before the onset of significant obesity or glucose dysregulation. Pancreata from 13-month-old Japanese macaques exposed to a HFD from in utero to necropsy were analyzed for expression of cytokines and islet-associated macrophages. Parameters from an intravenous glucose tolerance test were correlated with cytokine expression. Before significant glucose dysregulation, the HFD cohort had a twofold increase in interleukin 6 (IL6), associated with decreased first-phase insulin response and a sexually dimorphic (male) increase in IL1β correlating with increased fasting glucose levels. The number of islet-associated macrophages was also increased. Pancreata from juvenile NHP exposed to HFD have increased inflammatory markers and evidence of innate immune infiltration before the onset of significant obesity or glucose dysregulation. Given the parallel development of metabolic disease between humans and NHPs, these findings have strong relevance to the early metabolic disease driven by a chronic HFD in children.

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Zhiguo Liu Laboratory of Lipid and Glucose Metabolism, Laboratory of Metabolic Medicine, Division of Neuroscience, Department of Biochemistry, The First Affiliated Hospital of Chongqing Medical University, 1 Youyi Road, Yuzhong District, Chongqing 400016, People's Republic of China

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Chun Yan Lim Laboratory of Lipid and Glucose Metabolism, Laboratory of Metabolic Medicine, Division of Neuroscience, Department of Biochemistry, The First Affiliated Hospital of Chongqing Medical University, 1 Youyi Road, Yuzhong District, Chongqing 400016, People's Republic of China

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Michelle Yu-Fah Su Laboratory of Lipid and Glucose Metabolism, Laboratory of Metabolic Medicine, Division of Neuroscience, Department of Biochemistry, The First Affiliated Hospital of Chongqing Medical University, 1 Youyi Road, Yuzhong District, Chongqing 400016, People's Republic of China

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Stephanie Li Ying Soh Laboratory of Lipid and Glucose Metabolism, Laboratory of Metabolic Medicine, Division of Neuroscience, Department of Biochemistry, The First Affiliated Hospital of Chongqing Medical University, 1 Youyi Road, Yuzhong District, Chongqing 400016, People's Republic of China

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Guanghou Shui Laboratory of Lipid and Glucose Metabolism, Laboratory of Metabolic Medicine, Division of Neuroscience, Department of Biochemistry, The First Affiliated Hospital of Chongqing Medical University, 1 Youyi Road, Yuzhong District, Chongqing 400016, People's Republic of China

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Markus R Wenk Laboratory of Lipid and Glucose Metabolism, Laboratory of Metabolic Medicine, Division of Neuroscience, Department of Biochemistry, The First Affiliated Hospital of Chongqing Medical University, 1 Youyi Road, Yuzhong District, Chongqing 400016, People's Republic of China

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Kevin L Grove Laboratory of Lipid and Glucose Metabolism, Laboratory of Metabolic Medicine, Division of Neuroscience, Department of Biochemistry, The First Affiliated Hospital of Chongqing Medical University, 1 Youyi Road, Yuzhong District, Chongqing 400016, People's Republic of China

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George K Radda Laboratory of Lipid and Glucose Metabolism, Laboratory of Metabolic Medicine, Division of Neuroscience, Department of Biochemistry, The First Affiliated Hospital of Chongqing Medical University, 1 Youyi Road, Yuzhong District, Chongqing 400016, People's Republic of China

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Weiping Han Laboratory of Lipid and Glucose Metabolism, Laboratory of Metabolic Medicine, Division of Neuroscience, Department of Biochemistry, The First Affiliated Hospital of Chongqing Medical University, 1 Youyi Road, Yuzhong District, Chongqing 400016, People's Republic of China
Laboratory of Lipid and Glucose Metabolism, Laboratory of Metabolic Medicine, Division of Neuroscience, Department of Biochemistry, The First Affiliated Hospital of Chongqing Medical University, 1 Youyi Road, Yuzhong District, Chongqing 400016, People's Republic of China

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Xiaoqiu Xiao Laboratory of Lipid and Glucose Metabolism, Laboratory of Metabolic Medicine, Division of Neuroscience, Department of Biochemistry, The First Affiliated Hospital of Chongqing Medical University, 1 Youyi Road, Yuzhong District, Chongqing 400016, People's Republic of China
Laboratory of Lipid and Glucose Metabolism, Laboratory of Metabolic Medicine, Division of Neuroscience, Department of Biochemistry, The First Affiliated Hospital of Chongqing Medical University, 1 Youyi Road, Yuzhong District, Chongqing 400016, People's Republic of China

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Neonatal overnutrition results in accelerated development of high-fat diet (HFD)-induced metabolic defects in adulthood. To understand whether the increased susceptibility was associated with aggravated inflammation and dysregulated lipid metabolism, we studied metabolic changes and insulin signaling in a chronic postnatal overnutrition (CPO) mouse model. Male Swiss Webster pups were raised with either three pups per litter to induce CPO or ten pups per litter as control (CTR) and weaned to either low-fat diet (LFD) or HFD. All animals were killed on the postnatal day 150 (P150) except for a subset of mice killed on P15 for the measurement of stomach weight and milk composition. CPO mice exhibited accelerated body weight gain and increased body fat mass prior to weaning and the difference persisted into adulthood under conditions of both LFD and HFD. As adults, insulin signaling was more severely impaired in epididymal white adipose tissue (WAT) from HFD-fed CPO (CPO–HFD) mice. In addition, HFD-induced upregulation of pro-inflammatory cytokines was exaggerated in CPO–HFD mice. Consistent with greater inflammation, CPO–HFD mice showed more severe macrophage infiltration than HFD-fed CTR (CTR–HFD) mice. Furthermore, when compared with CTR–HFD mice, CPO–HFD mice exhibited reduced levels of several lipogenic enzymes in WAT and excess intramyocellular lipid accumulation. These data indicate that neonatal overnutrition accelerates the development of insulin resistance and exacerbates HFD-induced metabolic defects, possibly by worsening HFD-induced inflammatory response and impaired lipid metabolism.

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