Maynara L. Andrade

Av. Prof Lineu Prestes 1524
Sao Paulo, SP 05508000, Brazil

Last Updated: 09/26/2026

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Found 9 publications

Chloroquine attenuates diet-induced obesity and glucose intolerance through a mechanism that might involve FGF-21, but not UCP-1-mediated thermogenesis and inhibition of adipocyte autophagy.

Chloroquine attenuates diet-induced obesity and glucose intolerance through a mechanism that might involve FGF-21, but not UCP-1-mediated thermogenesis and inhibition of adipocyte autophagy.

Journal: Molecular and cellular endocrinology

Published: February 03, 2023

Adipocyte-specific mTORC2 deficiency impairs BAT and iWAT thermogenic capacity without affecting glucose uptake and energy expenditure in cold-acclimated mice.

Adipocyte-specific mTORC2 deficiency impairs BAT and iWAT thermogenic capacity without affecting glucose uptake and energy expenditure in cold-acclimated mice.

Journal: American journal of physiology. Endocrinology and metabolism

Published: September 20, 2021

PPARγ-induced upregulation of subcutaneous fat adiponectin secretion, glyceroneogenesis and BCAA oxidation requires mTORC1 activity.

PPARγ-induced upregulation of subcutaneous fat adiponectin secretion, glyceroneogenesis and BCAA oxidation requires mTORC1 activity.

Journal: Biochimica et biophysica acta. Molecular and cell biology of lipids

Published: January 29, 2021

Fish Oil Protects Wild Type and Uncoupling Protein 1-Deficient Mice from Obesity and Glucose Intolerance by Increasing Energy Expenditure.

Fish Oil Protects Wild Type and Uncoupling Protein 1-Deficient Mice from Obesity and Glucose Intolerance by Increasing Energy Expenditure.

Journal: Molecular nutrition & food research

Published: August 08, 2018

Constitutive Activation of the Nutrient Sensor mTORC1 in Myeloid Cells Induced by Tsc1 Deletion Protects Mice from Diet-Induced Obesity.

Constitutive Activation of the Nutrient Sensor mTORC1 in Myeloid Cells Induced by Tsc1 Deletion Protects Mice from Diet-Induced Obesity.

Journal: Molecular nutrition & food research

Published: March 22, 2018

PPARγ is a major regulator of branched-chain amino acid blood levels and catabolism in white and brown adipose tissues.

PPARγ is a major regulator of branched-chain amino acid blood levels and catabolism in white and brown adipose tissues.

Journal: Metabolism: clinical and experimental

Published: August 22, 2017

Adipocyte mTORC1 deficiency promotes adipose tissue inflammation and NLRP3 inflammasome activation via oxidative stress and de novo ceramide synthesis.

Adipocyte mTORC1 deficiency promotes adipose tissue inflammation and NLRP3 inflammasome activation via oxidative stress and de novo ceramide synthesis.

Journal: Journal of lipid research

Published: December 22, 2016

mTORC1 inhibition with rapamycin exacerbates adipose tissue inflammation in obese mice and dissociates macrophage phenotype from function.

mTORC1 inhibition with rapamycin exacerbates adipose tissue inflammation in obese mice and dissociates macrophage phenotype from function.

Journal: Immunobiology

Published: April 12, 2016

Constitutive adipocyte mTORC1 activation enhances mitochondrial activity and reduces visceral adiposity in mice.

Constitutive adipocyte mTORC1 activation enhances mitochondrial activity and reduces visceral adiposity in mice.

Journal: Biochimica et biophysica acta

Published: October 14, 2015

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Last Updated: 09/26/2026