KPV attenuates adipogenesis and lipid metabolism through modulation of ROS-mediated AKT/mTORC1/PPARγ signaling.

In mice with high-fat diet-induced obesity, oral KPV alleviated body weight gain.

In plain wordsIn mice fed a high-fat diet, oral KPV reduced body weight gain.

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In mice with high-fat diet-induced obesity, oral KPV alleviated white adipose tissue expansion.

In plain wordsIn mice fed a high-fat diet, oral KPV reduced growth of white fat tissue.

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In mice with high-fat diet-induced obesity, oral KPV alleviated the increase in liver mass.

In plain wordsIn mice fed a high-fat diet, oral KPV reduced the gain in liver weight.

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In mice with high-fat diet-induced obesity, oral KPV alleviated obesity-associated dyslipidemia.

In plain wordsIn mice fed a high-fat diet, oral KPV reduced abnormal blood fat levels.

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In mice with high-fat diet-induced obesity, oral KPV alleviated the elevation of plasma total cholesterol.

In plain wordsIn mice fed a high-fat diet, oral KPV reduced the rise in blood cholesterol.

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In 3T3-L1 preadipocytes, KPV suppressed MDI-induced adipocyte differentiation in a dose-dependent way.

In plain wordsIn lab tests on fat precursor cells, KPV reduced fat-cell formation, more strongly at higher doses.

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In 3T3-L1 preadipocytes, KPV at 100 μg/mL reduced Oil Red O staining by about 55% compared with MDI-treated cells.

In plain wordsIn lab tests on fat precursor cells, KPV lowered fat staining compared with untreated differentiating cells.

Measurements

Oil Red O staining reduction

≈ 55%

KPV 100 μg/mL vs MDI-treated

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In 3T3-L1 preadipocytes, KPV at 100 μg/mL reduced intracellular triglyceride by about 38% compared with MDI-treated cells.

In plain wordsIn lab tests on fat precursor cells, KPV lowered stored fat compared with untreated differentiating cells.

Measurements

Triglyceride content reduction

≈ 38%

KPV 100 μg/mL vs MDI-treated

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In 3T3-L1 preadipocytes, KPV decreased expression of the adipogenic marker PPARγ.

In plain wordsIn lab tests on fat precursor cells, KPV lowered a key protein that drives fat-cell formation.

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In 3T3-L1 preadipocytes, KPV decreased expression of the adipogenic marker fatty acid synthase (FAS).

In plain wordsIn lab tests on fat precursor cells, KPV lowered a fat-making enzyme.

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In differentiating 3T3-L1 cells, KPV attenuated reactive oxygen species production.

In plain wordsIn lab tests on fat precursor cells, KPV lowered production of reactive oxygen species.

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In differentiating 3T3-L1 cells, KPV treatment was associated with reduced AKT-dependent mTOR signaling.

In plain wordsIn lab tests on fat precursor cells, KPV was linked to weaker AKT and mTOR signals.

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In differentiating 3T3-L1 cells, KPV was associated with altered PPARγ phosphorylation; the direction is not stated.

In plain wordsIn lab tests on fat precursor cells, KPV was linked to a change in PPARγ phosphorylation.

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