Abstract
LPIN1 is a gene with important effects on lipidic and metabolic homeostasis. Human subcutaneous LPIN1 expression levels in adipose tissue are related with a better metabolic profile, including insulin sensitivity markers. However, there are few data on the regulation of LPIN1 in visceral adipose tissue (VAT). Our aim was to perform a cross-sectional analysis of VAT compared with subcutaneous (SAT) LPIN1 expression in a well-characterized obese cohort, its relation with the expression of genes involved in lipid metabolism, and the in vitro response to lipogenic and lipolytic stimuli. A downregulation of total LPIN1 mRNA expression in subjects with obesity was found in VAT similarly to that in SAT. Despite similar total LPIN1 mRNA levels in SAT and VAT, a close relationship with clinical parameters and with many lipogenic and lipolytic genes was observed primarily in SAT depot. As shown in the in vitro analysis, the low-grade proinflammatory environment and the insulin resistance associated with obesity may contribute to downregulate LPIN1 in adipose tissue, leading to a worse metabolic profile.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adipocytes / drug effects
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Adipocytes / metabolism
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Adipose Tissue / cytology
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Adipose Tissue / drug effects
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Adipose Tissue / metabolism*
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Adrenergic beta-Agonists / pharmacology
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Adult
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Aged
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Blotting, Western
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Body Mass Index
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Cell Differentiation
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Cells, Cultured
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Cohort Studies
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Cross-Sectional Studies
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DNA, Complementary / biosynthesis
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DNA, Complementary / genetics
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Female
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Gene Expression / genetics
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Humans
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Hypoglycemic Agents / pharmacology
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Insulin / pharmacology
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Isoproterenol / pharmacology
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Lipid Metabolism / drug effects
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Lipid Metabolism / genetics*
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Lipolysis / drug effects
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Lipolysis / genetics*
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Male
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Metabolic Syndrome / metabolism
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Middle Aged
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Nuclear Proteins / biosynthesis*
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Nuclear Proteins / genetics
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Phosphatidate Phosphatase
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Subcutaneous Fat / cytology
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Subcutaneous Fat / drug effects
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Subcutaneous Fat / metabolism*
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Tumor Necrosis Factor-alpha / pharmacology
Substances
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Adrenergic beta-Agonists
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DNA, Complementary
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Hypoglycemic Agents
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Insulin
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Nuclear Proteins
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Tumor Necrosis Factor-alpha
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LPIN1 protein, human
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Phosphatidate Phosphatase
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Isoproterenol