Pancreatic inflammation and increased islet macrophages in insulin-resistant juvenile primates
Open accessAbstract
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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Obesity is frequently characterized by systemic inflammation, and preclinical evidence links systemic inflammation to β-cell dysfunction.
“Obesity is frequently characterized by systemic inflammation and preclinical evidence links systemic inflammation to β-cell dysfunction63,64.”
From Pathophysiology and treatment of type 2 diabetes: perspectives on the past, present, and future (2014) · cites this paper as [64]
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- Authors
- Nicol, L. E., Grant, W. F., Comstock, S. M., Nguyen, M. L., Smith, M. S., Grove, K. L., & Marks, D. L.
- Affiliations
- Oregon National Primate Research Center (US)
- Oregon Health & Science University (US)
- Venue
- Journal of Endocrinology
- Publisher
- Bioscientifica
- Published
- 2013-02-18
- Volume
- 217
- Issue
- 2
- Pages
- 207-213
- ISSN
- 0022-0795 (ISSN-L)
- 1479-6805
- PMC
- PMC3697080
- OpenAlex
- W2142885090
- Cited by
- 44
- References
- 30
- Citations by year
- 2025: 1 · 2024: 1 · 2023: 4 · 2022: 4 · 2021: 4 · 2020: 3 · 2019: 3 · 2018: 5 · 2016: 7 · 2015: 4 · 2014: 5 · 2013: 3
- FWCI
- 6.24
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Endocrinology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Burroughs Wellcome Fund (1007518)
- Oregon Health and Science University
- National Institutes of Health (P51OD011092)
- Oregon National Primate Research Center
- National Institute of Diabetes and Digestive and Kidney Diseases (R24DK090964, R01DK079194, P30DK020593)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (R01HD014643, K12HD057588)
- Topics
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
- Keywords
- pancreatitis, insulin resistance, childhood obesity, type 2 diabetes, innate immunity, interleukin-6, IL-1β, Japanese macaque, juvenile primates, first-phase insulin response, sex differences, glucose tolerance
- MeSH terms
- Animals, Blood Glucose, Disease Models, Animal, Female, Insulin Resistance, Islets of Langerhans, Macaca, Macrophages, Male, Pancreatitis, Sex Factors, Interleukin-6, Interleukin-1beta, Diet, High-Fat
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