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Article ; Online: In vivo techniques for assessment of insulin sensitivity and glucose metabolism.

Hahn, Margaret K / Giacca, Adria / Pereira, Sandra

2024 Volume 260, Issue 3

Abstract: Metabolic tests are vital to determine in vivo insulin sensitivity and glucose metabolism in preclinical models, usually rodents. Such tests include glucose tolerance tests, insulin tolerance tests, and glucose clamps. Although these tests are not ... ...

Abstract	Metabolic tests are vital to determine in vivo insulin sensitivity and glucose metabolism in preclinical models, usually rodents. Such tests include glucose tolerance tests, insulin tolerance tests, and glucose clamps. Although these tests are not standardized, there are general guidelines for their completion and analysis that are constantly being refined. In this review, we describe metabolic tests in rodents as well as factors to consider when designing and performing these tests.
MeSH term(s)	Humans ; Insulin Resistance ; Blood Glucose/metabolism ; Glucose Tolerance Test ; Glucose Clamp Technique ; Insulin/metabolism
Chemical Substances	Blood Glucose ; Insulin
Language	English
Publishing date	2024-01-31
Publishing country	England
Document type	Review ; Journal Article
ZDB-ID	3028-4
ISSN	1479-6805 ; 0022-0795
ISSN (online)	1479-6805
ISSN	0022-0795
DOI	10.1530/JOE-23-0308
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Article ; Online: Role of c-Jun N-terminal Kinase (JNK) in Obesity and Type 2 Diabetes.

Yung, Justin Hou Ming / Giacca, Adria

Cells

2020 Volume 9, Issue 3

Abstract: Obesity has been described as a global epidemic and is a low-grade chronic inflammatory disease that arises as a consequence of energy imbalance. Obesity increases the risk of type 2 diabetes (T2D), by mechanisms that are not entirely clarified. Elevated ...

Abstract	Obesity has been described as a global epidemic and is a low-grade chronic inflammatory disease that arises as a consequence of energy imbalance. Obesity increases the risk of type 2 diabetes (T2D), by mechanisms that are not entirely clarified. Elevated circulating pro-inflammatory cytokines and free fatty acids (FFA) during obesity cause insulin resistance and ß-cell dysfunction, the two main features of T2D, which are both aggravated with the progressive development of hyperglycemia. The inflammatory kinase c-jun N-terminal kinase (JNK) responds to various cellular stress signals activated by cytokines, free fatty acids and hyperglycemia, and is a key mediator in the transition between obesity and T2D. Specifically, JNK mediates both insulin resistance and ß-cell dysfunction, and is therefore a potential target for T2D therapy.
MeSH term(s)	Diabetes Mellitus, Type 2/drug therapy ; Diabetes Mellitus, Type 2/metabolism ; Diabetes Mellitus, Type 2/pathology ; Fatty Acids, Nonesterified/metabolism ; Glucose/metabolism ; Humans ; Inflammation ; Insulin Resistance ; Insulin Secretion ; JNK Mitogen-Activated Protein Kinases/antagonists & inhibitors ; JNK Mitogen-Activated Protein Kinases/genetics ; JNK Mitogen-Activated Protein Kinases/metabolism ; Obesity/drug therapy ; Obesity/metabolism ; Obesity/pathology ; Protein Kinase Inhibitors/therapeutic use
Chemical Substances	Fatty Acids, Nonesterified ; Protein Kinase Inhibitors ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2020-03-13
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells9030706
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Article ; Online: Hydrogel Microneedle-Assisted Assay Integrating Aptamer Probes and Fluorescence Detection for Reagentless Biomarker Quantification.

Zheng, Hanjia / GhavamiNejad, Amin / GhavamiNejad, Peyman / Samarikhalaj, Melisa / Giacca, Adria / Poudineh, Mahla

ACS sensors

2022 Volume 7, Issue 8, Page(s) 2387–2399

Abstract: Analyzing interstitial fluid (ISF) via microneedle (MN) devices enables patient health monitoring in a minimally invasive manner and in point-of-care settings. However, most MN-based diagnostic approaches require complicated fabrication processes and ... ...

Abstract	Analyzing interstitial fluid (ISF) via microneedle (MN) devices enables patient health monitoring in a minimally invasive manner and in point-of-care settings. However, most MN-based diagnostic approaches require complicated fabrication processes and postprocessing of the extracted ISF or are limited to detection of electrochemically active biomarkers. Here, we show on-needle measurement of target analytes by integrating hydrogel microneedles with aptamer probes as the recognition elements. Fluorescently tagged aptamer probes are chemically attached to the hydrogel matrix using a simple and novel approach, while a cross-linked patch is formed. For reagentless detection, we employ a strand displacement strategy where fluorophore-conjugated aptamers are hybridized with a DNA competitor strand conjugated to a quencher molecule. The assay is utilized for rapid (2 min) measurement of glucose, adenosine triphosphate, l-tyrosinamide, and thrombin ex vivo. Furthermore, the system enables specific and sensitive quantification of rising and falling concentrations of glucose in an animal model of diabetes to track hypoglycemia, euglycemia, and hyperglycemia conditions. Our assay can be applied for rapid measurement of a diverse range of biomarkers, proteins, or small molecules, introducing a generalizable platform for biomolecule quantification, and has the potential to improve the quality of life of patients who are in need of close monitoring of biomarkers of health and disease.
MeSH term(s)	Animals ; Biomarkers ; Fluorescence ; Glucose ; Hydrogels ; Oligonucleotides ; Quality of Life
Chemical Substances	Biomarkers ; Hydrogels ; Oligonucleotides ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2022-07-22
Publishing country	United States
Document type	Journal Article
ISSN	2379-3694
ISSN (online)	2379-3694
DOI	10.1021/acssensors.2c01033
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Article ; Online: "Smart" Matrix Microneedle Patch Made of Self-Crosslinkable and Multifunctional Polymers for Delivering Insulin On-Demand.

Liu, Jackie Fule / GhavamiNejad, Amin / Lu, Brian / Mirzaie, Sako / Samarikhalaj, Melisa / Giacca, Adria / Wu, Xiao Yu

Advanced science (Weinheim, Baden-Wurttemberg, Germany)

2023 Volume 10, Issue 30, Page(s) e2303665

Abstract: A transdermal patch that delivers insulin at high glucose concentrations can offer tremendous advantages to ease the concern of safety and improve the quality of life for people with diabetes. Herein, a novel self-crosslinkable and glucose-responsive ... ...

Abstract	A transdermal patch that delivers insulin at high glucose concentrations can offer tremendous advantages to ease the concern of safety and improve the quality of life for people with diabetes. Herein, a novel self-crosslinkable and glucose-responsive polymer-based microneedle patch (MN) is designed to deliver insulin at hyperglycemia. The microneedle patch is made of hyaluronic acid polymers functionalized with dopamine and 4-amino-3-fluorophenylboronic acid (AFBA) that can be quickly crosslinked upon mixing of the polymer solutions in the absence of any chemicalcrosslinking agents or organic solvents. The catechol groups in the dopamine (DA) units form covalent crosslinkages among themselves by auto-oxidation and dynamic crosslink with phenylboronic acid (PBA) via complexation. The reversible crosslinkages between catechol and boronate decrease with increasing glucose concentration leading to higher swelling and faster insulin release at hyperglycemia as compared to euglycemia. Such superior glucose-responsive properties are demonstrated by in vitro analyses and in vivo efficacy studies. The hydrogel polymers also preserve native structure and bioactivity of insulin, attributable to the interaction of hyaluronic acid (HA) with insulin molecules, as revealed by experiments and molecular dynamics simulations. The simplicity in the design and fabrication process, and glucose-responsiveness in insulin delivery impart the matrix microneedle (mMN) patch great potential for clinical translation.
MeSH term(s)	Animals ; Humans ; Insulin/chemistry ; Blood Glucose/analysis ; Hyaluronic Acid/chemistry ; Polymers/chemistry ; Dopamine ; Quality of Life ; Diabetes Mellitus, Experimental/drug therapy ; Glucose ; Hyperglycemia
Chemical Substances	Insulin ; Blood Glucose ; Hyaluronic Acid (9004-61-9) ; Polymers ; Dopamine (VTD58H1Z2X) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2023-09-18
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2808093-2
ISSN	2198-3844 ; 2198-3844
ISSN (online)	2198-3844
ISSN	2198-3844
DOI	10.1002/advs.202303665
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Article ; Online: Olanzapine's effects on hypothalamic transcriptomics and kinase activity.

Pereira, Sandra / Castellani, Laura N / Kowalchuk, Chantel / Alganem, Khaled / Zhang, Xiaolu / Ryan, William G / Singh, Raghunath / Wu, Sally / Au, Emily / Asgariroozbehani, Roshanak / Agarwal, Sri Mahavir / Giacca, Adria / Mccullumsmith, Robert E / Hahn, Margaret K

Psychoneuroendocrinology

2024 Volume 163, Page(s) 106987

Abstract: Olanzapine is a second-generation antipsychotic that disrupts metabolism and is associated with an increased risk of type 2 diabetes. The hypothalamus is a key region in the control of whole-body metabolic homeostasis. The objective of the current study ... ...

Abstract	Olanzapine is a second-generation antipsychotic that disrupts metabolism and is associated with an increased risk of type 2 diabetes. The hypothalamus is a key region in the control of whole-body metabolic homeostasis. The objective of the current study was to determine how acute peripheral olanzapine administration affects transcription and serine/threonine kinase activity in the hypothalamus. Hypothalamus samples from rats were collected following the pancreatic euglycemic clamp, thereby allowing us to study endpoints under steady state conditions for plasma glucose and insulin. Olanzapine stimulated pathways associated with inflammation, but diminished pathways associated with the capacity to combat endoplasmic reticulum stress and G protein-coupled receptor activity. These pathways represent potential targets to reduce the incidence of type 2 diabetes in patients taking antipsychotics.
MeSH term(s)	Humans ; Rats ; Animals ; Olanzapine/pharmacology ; Olanzapine/metabolism ; Diabetes Mellitus, Type 2/drug therapy ; Diabetes Mellitus, Type 2/metabolism ; Benzodiazepines/pharmacology ; Benzodiazepines/metabolism ; Antipsychotic Agents/pharmacology ; Antipsychotic Agents/metabolism ; Hypothalamus/metabolism ; Gene Expression Profiling
Chemical Substances	Olanzapine (N7U69T4SZR) ; Benzodiazepines (12794-10-4) ; Antipsychotic Agents
Language	English
Publishing date	2024-02-06
Publishing country	England
Document type	Journal Article
ZDB-ID	197636-9
ISSN	1873-3360 ; 0306-4530
ISSN (online)	1873-3360
ISSN	0306-4530
DOI	10.1016/j.psyneuen.2024.106987
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Article ; Online: Carnosic Acid Attenuates the Free Fatty Acid-Induced Insulin Resistance in Muscle Cells and Adipocytes.

Den Hartogh, Danja J / Vlavcheski, Filip / Giacca, Adria / MacPherson, Rebecca E K / Tsiani, Evangelia

Cells

2022 Volume 11, Issue 1

Abstract: Elevated blood free fatty acids (FFAs), as seen in obesity, impair insulin action leading to insulin resistance and Type 2 diabetes mellitus. Several serine/threonine kinases including JNK, mTOR, and p70 S6K cause serine phosphorylation of the insulin ... ...

Abstract	Elevated blood free fatty acids (FFAs), as seen in obesity, impair insulin action leading to insulin resistance and Type 2 diabetes mellitus. Several serine/threonine kinases including JNK, mTOR, and p70 S6K cause serine phosphorylation of the insulin receptor substrate (IRS) and have been implicated in insulin resistance. Activation of AMP-activated protein kinase (AMPK) increases glucose uptake, and in recent years, AMPK has been viewed as an important target to counteract insulin resistance. We reported previously that carnosic acid (CA) found in rosemary extract (RE) and RE increased glucose uptake and activated AMPK in muscle cells. In the present study, we examined the effects of CA on palmitate-induced insulin-resistant L6 myotubes and 3T3L1 adipocytes. Exposure of cells to palmitate reduced the insulin-stimulated glucose uptake, GLUT4 transporter levels on the plasma membrane, and Akt activation. Importantly, CA attenuated the deleterious effect of palmitate and restored the insulin-stimulated glucose uptake, the activation of Akt, and GLUT4 levels. Additionally, CA markedly attenuated the palmitate-induced phosphorylation/activation of JNK, mTOR, and p70S6K and activated AMPK. Our data indicate that CA has the potential to counteract the palmitate-induced muscle and fat cell insulin resistance.
MeSH term(s)	3T3-L1 Cells ; AMP-Activated Protein Kinases/metabolism ; Abietanes/pharmacology ; Adipocytes/drug effects ; Adipocytes/pathology ; Animals ; Cell Line ; Fatty Acids, Nonesterified/toxicity ; Glucose/metabolism ; Insulin/pharmacology ; Insulin Receptor Substrate Proteins/metabolism ; Insulin Resistance ; JNK Mitogen-Activated Protein Kinases/metabolism ; Mice ; Models, Biological ; Muscle Cells/drug effects ; Muscle Cells/pathology ; Muscle Fibers, Skeletal/drug effects ; Muscle Fibers, Skeletal/metabolism ; Palmitates/toxicity ; Phosphorylation/drug effects ; Phosphoserine/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Rats ; Ribosomal Protein S6 Kinases, 70-kDa/metabolism ; TOR Serine-Threonine Kinases/metabolism
Chemical Substances	Abietanes ; Fatty Acids, Nonesterified ; Insulin ; Insulin Receptor Substrate Proteins ; Palmitates ; Phosphoserine (17885-08-4) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Ribosomal Protein S6 Kinases, 70-kDa (EC 2.7.11.1) ; TOR Serine-Threonine Kinases (EC 2.7.11.1) ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; AMP-Activated Protein Kinases (EC 2.7.11.31) ; Glucose (IY9XDZ35W2) ; salvin (LI791SXT24)
Language	English
Publishing date	2022-01-05
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells11010167
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Article ; Online: Role of c-Jun N-terminal Kinase (JNK) in Obesity and Type 2 Diabetes

Justin Hou Ming Yung / Adria Giacca

Cells, Vol 9, Iss 3, p

2020 Volume 706

Abstract	Obesity has been described as a global epidemic and is a low-grade chronic inflammatory disease that arises as a consequence of energy imbalance. Obesity increases the risk of type 2 diabetes (T2D), by mechanisms that are not entirely clarified. Elevated circulating pro-inflammatory cytokines and free fatty acids (FFA) during obesity cause insulin resistance and ß-cell dysfunction, the two main features of T2D, which are both aggravated with the progressive development of hyperglycemia. The inflammatory kinase c-jun N-terminal kinase (JNK) responds to various cellular stress signals activated by cytokines, free fatty acids and hyperglycemia, and is a key mediator in the transition between obesity and T2D. Specifically, JNK mediates both insulin resistance and ß-cell dysfunction, and is therefore a potential target for T2D therapy.
Keywords	c-jun n-terminal kinase ; jnk ; type 2 diabetes ; inflammation ; obesity ; insulin resistance ; lipotoxicity ; glucotoxicity ; Biology (General) ; QH301-705.5
Subject code	571
Language	English
Publishing date	2020-03-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: β-Cell Insulin Resistance Plays a Causal Role in Fat-Induced β-Cell Dysfunction In Vitro and In Vivo.

Ivovic, Aleksandar / Yung, Justin Hou Ming / Oprescu, Andrei I / Vlavcheski, Filip / Mori, Yusaku / Rahman, S M Niazur / Ye, Wenyue / Eversley, Judith A / Wheeler, Michael B / Woo, Minna / Tsiani, Evangelia / Giacca, Adria

Endocrinology

2024 Volume 165, Issue 5

Abstract: In the classical insulin target tissues of liver, muscle, and adipose tissue, chronically elevated levels of free fatty acids (FFA) impair insulin signaling. Insulin signaling molecules are also present in β-cells where they play a role in β-cell ... ...

Abstract	In the classical insulin target tissues of liver, muscle, and adipose tissue, chronically elevated levels of free fatty acids (FFA) impair insulin signaling. Insulin signaling molecules are also present in β-cells where they play a role in β-cell function. Therefore, inhibition of the insulin/insulin-like growth factor 1 pathway may be involved in fat-induced β-cell dysfunction. To address the role of β-cell insulin resistance in FFA-induced β-cell dysfunction we co-infused bisperoxovanadate (BPV) with oleate or olive oil for 48 hours in rats. BPV, a tyrosine phosphatase inhibitor, acts as an insulin mimetic and is devoid of any antioxidant effect that could prevent β-cell dysfunction, unlike most insulin sensitizers. Following fat infusion, rats either underwent hyperglycemic clamps for assessment of β-cell function in vivo or islets were isolated for ex vivo assessment of glucose-stimulated insulin secretion (GSIS). We also incubated islets with oleate or palmitate and BPV for in vitro assessment of GSIS and Akt (protein kinase B) phosphorylation. Next, mice with β-cell specific deletion of PTEN (phosphatase and tensin homolog; negative regulator of insulin signaling) and littermate controls were infused with oleate for 48 hours, followed by hyperglycemic clamps or ex vivo evaluation of GSIS. In rat experiments, BPV protected against fat-induced impairment of β-cell function in vivo, ex vivo, and in vitro. In mice, β-cell specific deletion of PTEN protected against oleate-induced β-cell dysfunction in vivo and ex vivo. These data support the hypothesis that β-cell insulin resistance plays a causal role in FFA-induced β-cell dysfunction.
MeSH term(s)	Animals ; Insulin Resistance/physiology ; Insulin-Secreting Cells/drug effects ; Insulin-Secreting Cells/metabolism ; Rats ; Mice ; Male ; PTEN Phosphohydrolase/metabolism ; Oleic Acid/pharmacology ; Insulin/metabolism ; Mice, Inbred C57BL ; Insulin Secretion/drug effects ; Fatty Acids, Nonesterified/metabolism ; Rats, Sprague-Dawley
Chemical Substances	PTEN Phosphohydrolase (EC 3.1.3.67) ; Oleic Acid (2UMI9U37CP) ; Insulin ; Fatty Acids, Nonesterified
Language	English
Publishing date	2024-04-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/endocr/bqae044
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Article ; Online: NOD1: An Interface Between Innate Immunity and Insulin Resistance.

Rivers, Sydney L / Klip, Amira / Giacca, Adria

Endocrinology

2019 Volume 160, Issue 5, Page(s) 1021–1030

Abstract: Insulin resistance is driven, in part, by activation of the innate immune system. We have discussed the evidence linking nucleotide-binding oligomerization domain (NOD)1, an intracellular pattern recognition receptor, to the onset and progression of ... ...

Abstract	Insulin resistance is driven, in part, by activation of the innate immune system. We have discussed the evidence linking nucleotide-binding oligomerization domain (NOD)1, an intracellular pattern recognition receptor, to the onset and progression of obesity-induced insulin resistance. On a molecular level, crosstalk between downstream NOD1 effectors and the insulin receptor pathway inhibits insulin signaling, potentially through reduced insulin receptor substrate action. In vivo studies have demonstrated that NOD1 activation induces peripheral, hepatic, and whole-body insulin resistance. Also, NOD1-deficient models are protected from high-fat diet (HFD)-induced insulin resistance. Moreover, hematopoietic NOD1 deficiency prevented HFD-induced changes in proinflammatory macrophage polarization status, thus protecting against the development of metabolic inflammation and insulin resistance. Serum from HFD-fed mice activated NOD1 signaling ex vivo; however, the molecular identity of the activating factors remains unclear. Many have proposed that an HFD changes the gut permeability, resulting in increased translocation of bacterial fragments and increased circulating NOD1 ligands. In contrast, others have suggested that NOD1 ligands are endogenous and potentially lipid-derived metabolites produced during states of nutrient overload. Nevertheless, that NOD1 contributes to the development of insulin resistance, and that NOD1-based therapy might provide benefit, is an exciting advancement in metabolic research.
MeSH term(s)	Animals ; Diet, High-Fat ; Immunity, Innate/genetics ; Immunity, Innate/immunology ; Inflammation/genetics ; Inflammation/immunology ; Inflammation/metabolism ; Insulin Resistance/immunology ; Mice ; Models, Immunological ; Nod1 Signaling Adaptor Protein/genetics ; Nod1 Signaling Adaptor Protein/immunology ; Nod1 Signaling Adaptor Protein/metabolism ; Obesity/genetics ; Obesity/immunology ; Obesity/metabolism ; Receptor, Insulin/metabolism ; Signal Transduction/genetics ; Signal Transduction/immunology
Chemical Substances	Nod1 Signaling Adaptor Protein ; Nod1 protein, mouse ; Receptor, Insulin (EC 2.7.10.1)
Language	English
Publishing date	2019-02-26
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/en.2018-01061
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Article ; Online: Attenuation of Free Fatty Acid (FFA)-Induced Skeletal Muscle Cell Insulin Resistance by Resveratrol is Linked to Activation of AMPK and Inhibition of mTOR and p70 S6K.

Den Hartogh, Danja J / Vlavcheski, Filip / Giacca, Adria / Tsiani, Evangelia

International journal of molecular sciences

2020 Volume 21, Issue 14

Abstract: Insulin resistance, a main characteristic of type 2 diabetes mellitus (T2DM), is linked to obesity and excessive levels of plasma free fatty acids (FFA). Studies indicated that significantly elevated levels of FFAs lead to skeletal muscle insulin ... ...

Abstract	Insulin resistance, a main characteristic of type 2 diabetes mellitus (T2DM), is linked to obesity and excessive levels of plasma free fatty acids (FFA). Studies indicated that significantly elevated levels of FFAs lead to skeletal muscle insulin resistance, by dysregulating the steps in the insulin signaling cascade. The polyphenol resveratrol (RSV) was shown to have antidiabetic properties but the exact mechanism(s) involved are not clearly understood. In the present study, we examined the effect of RSV on FFA-induced insulin resistance in skeletal muscle cells in vitro and investigated the mechanisms involved. Parental and GLUT4myc-overexpressing L6 rat skeletal myotubes were used. [
MeSH term(s)	Adenylate Kinase/physiology ; Animals ; Cell Line ; Fatty Acids, Nonesterified/toxicity ; Glucose/metabolism ; Glucose Transporter Type 4/metabolism ; Humans ; Insulin Receptor Substrate Proteins/metabolism ; Insulin Resistance/physiology ; Muscle Cells/drug effects ; Muscle Cells/metabolism ; Muscle, Skeletal/drug effects ; Muscle, Skeletal/metabolism ; Palmitates/pharmacology ; Palmitates/toxicity ; Phosphorylation ; Protein Processing, Post-Translational/drug effects ; Protein Transport/drug effects ; Rats ; Resveratrol/pharmacology ; Ribosomal Protein S6 Kinases, 70-kDa/physiology ; Signal Transduction/drug effects ; TOR Serine-Threonine Kinases/physiology
Chemical Substances	Fatty Acids, Nonesterified ; Glucose Transporter Type 4 ; Insulin Receptor Substrate Proteins ; Irs1 protein, rat ; Palmitates ; Slc2a4 protein, rat ; MTOR protein, human (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; Ribosomal Protein S6 Kinases, 70-kDa (EC 2.7.11.1) ; Adenylate Kinase (EC 2.7.4.3) ; Glucose (IY9XDZ35W2) ; Resveratrol (Q369O8926L)
Language	English
Publishing date	2020-07-11
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms21144900
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