ArticleObesity (Silver Spring, Md.)2016
Effects of glucose and insulin on secretion of amyloid-β by human adipose tissue cells.
Article in Obesity (Silver Spring, Md.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- A Question of Origins: Non-neuronal Sources of Amyloid-β.Neuroscience bulletin · 2026Review
- Sexual dimorphism in obesity is governed by RELMα regulation of adipose macrophages and eosinophils.eLife · 2023Article
- The Effect of the Sodium-Glucose Cotransporter Inhibitor on Cognition and Metabolic Parameters in a Rat Model of Sporadic Alzheimer's Disease.Biomedicines · 2023Article
- Sexual dimorphism in obesity is governed by RELMα regulation of adipose macrophages and eosinophils.bioRxiv : the preprint server for biology · 2023Article
- Linking Diabetes to Alzheimer's Disease: Potential Roles of Glucose Metabolism and Alpha-Glucosidase.Current neuropharmacology · 2023Review
- Effect of Obesity and High-Density Lipoprotein Concentration on the Pathological Characteristics of Alzheimer's Disease in High-Fat Diet-Fed Mice.International journal of molecular sciences · 2022Article
- Brain Mitochondrial Dysfunction: A Possible Mechanism Links Early Life Anxiety to Alzheimer's Disease in Later Life.Aging and disease · 2022Article
- Peripheral Aβ acts as a negative modulator of insulin secretion.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Relationship of fasting glucose and longitudinal Alzheimer's disease imaging markers.Alzheimer's & dementia (New York, N. Y.) · 2022Article
- Distribution and inter-regional relationship of amyloid-beta plaque deposition in a 5xFAD mouse model of Alzheimer's disease.Frontiers in aging neuroscience · 2022Article
- The Other Side of Alzheimer's Disease: Influence of Metabolic Disorder Features for Novel Diagnostic Biomarkers.Journal of personalized medicine · 2020Review
- The Interplay between Diabetes and Alzheimer's Disease-In the Hunt for Biomarkers.International journal of molecular sciences · 2020Review
- γ-Secretase Modulatory Proteins: The Guiding Hand Behind the Running Scissors.Frontiers in aging neuroscience · 2020Article
- Amyloid precursor protein modulates macrophage phenotype and diet-dependent weight gain.Scientific reports · 2017Article
- Measurement of altered APP isoform expression in adipose tissue of diet-induced obese mice by absolute quantitative real-time PCR.Animal cells and systems · 2017Article
- Type 2 diabetes mellitus in the pathophysiology of Alzheimer's disease.Dementia & neuropsychologiaArticle
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
objectiveObesity and type 2 diabetes mellitus are risk factors for developing Alzheimer disease. Overlapping patterns of metabolic dysfunction may be common molecular links between these complex diseases. Amyloid-β (Aβ) precursor protein and associated β- and γ-secretases are expressed in adipose tissue. Aβ precursor protein is up-regulated with obesity and correlated to insulin resistance. Aβ may be secreted by adipose tissue, its production may be regulated through metabolic pathways, and Aβ may exert effects on adipose tissue insulin receptor signaling.
methodsHuman stromal-vascular cells and differentiated adipocytes were cultured with different combinations of glucose and insulin and then assayed for Aβ in conditioned media. Aβ was measured in vivo using adipose tissue microdialysis.
resultsAβ secretion was increased by glucose and insulin in vitro. Adipose tissue microdialysates contained Aβ. Adipocytes treated with Aβ had decreased expression of insulin receptor substrate-2 and reduced Akt-1 phosphorylation.
conclusionsAβ was made by adipose tissue cells in vitro at concentrations similar to in vivo measurements. Regulation of Aβ production by glucose and insulin and effects of Aβ on the insulin receptor pathway suggest similar cellular mechanisms may exist between neuronal dysfunction in Alzheimer disease and adipose dysfunction in type 2 diabetes.
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