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Article: Altered Sympathoadrenal Activity Following Cold-Water Diving.

Kelly, Karen R / Pautz, Carina M / Palombo, Laura J / Jensen, Andrew E / Melau, Jorgen / Turcotte, Lorraine P / Solberg, Paul A

Journal of special operations medicine : a peer reviewed journal for SOF medical professionals

2023 Volume 23, Issue 3, Page(s) 74–81

Abstract: ... maintained (p > .05), whereas skin temperature was significantly reduced over the course of each dive (p ... significantly decreased across both dives and days (p < .001). Adrenaline and noradrenaline significantly ... increased across both time and day (p < .001). Leptin, testosterone, and IGF-1 significantly decreased over ...

Abstract	Introduction: Little data exist on the effect of extremely cold-water diving on thermo-metabolic hormone secretion. Moreover, the impact of repetitive dives on the stress response is unknown. The purpose of this study was to determine the effects of two daily bouts of cold-water diving on the hormonal and metabolic profile of elite military personnel and to measure the stress response. Methods: Healthy, male, Norwegian Special Forces operators (n = 5) volunteered for this study. Physiological and hormone data were analyzed prior to and following twice-daily Arctic dives (3.3°C). Results: Core temperature was maintained (p > .05), whereas skin temperature was significantly reduced over the course of each dive (p < .01). Pairwise comparisons revealed adrenocorticotropic hormone (ACTH) and cortisol concentration significantly decreased across both dives and days (p < .001). Adrenaline and noradrenaline significantly increased across both time and day (p < .001). Leptin, testosterone, and IGF-1 significantly decreased over time but recovered between days. Conclusion: The main findings of this effort are that there is a rapid sympathetic-adreno-medullary (SAM/SNS) response to cold-water diving and a suppression of the hypothalamic-pituitary-adrenal (HPA) axis and hormones related to repair and recovery. While the sample size was too small to determine the role of SAM/SNS, HPA, and thyroid hormone effect on thermoregulation, it addresses a gap in our understanding of physiological adaptions that occurs in extreme environments.
MeSH term(s)	Humans ; Male ; Diving ; Cold Temperature ; Adrenocorticotropic Hormone ; Epinephrine ; Water
Chemical Substances	Adrenocorticotropic Hormone (9002-60-2) ; Epinephrine (YKH834O4BH) ; Water (059QF0KO0R)
Language	English
Publishing date	2023-07-25
Publishing country	United States
Document type	Journal Article
ZDB-ID	3006517-3
ISSN	1553-9768
ISSN	1553-9768
DOI	10.55460/T5CZ-JXVK
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Article ; Online: Hormonal balance and nutritional intake in elite tactical athletes.

Jensen, Andrew E / Arrington, Laura J / Turcotte, Lorraine P / Kelly, Karen R

Steroids

2019 Volume 152, Page(s) 108504

Abstract: Chronic exposure to multifactorial stress, such as that endured by elite military operators, may lead to overtraining syndrome and negatively impact hormonal regulation. In acute settings (<6 mos), military training has been shown to lead to hormonal ... ...

Abstract	Chronic exposure to multifactorial stress, such as that endured by elite military operators, may lead to overtraining syndrome and negatively impact hormonal regulation. In acute settings (<6 mos), military training has been shown to lead to hormonal dysfunction; however, less is known about the consequences of long-term military training. Thus, the purpose of this study was to determine the chronic effects of military operations and training on the hormone profile of elite military operators. A cross-sectional, random sample of active duty elite US military operators (n = 65, age = 29.8 ± 1.0 yrs, height = 178.4 ± 0.7 cm, weight = 85.1 ± 2.0 kg) concomitantly engaged in rigorous physical training were recruited to participate in the study. Following an overnight fast, waking plasma concentrations of luteinizing hormone, total testosterone (TT), free testosterone, sex-hormone binding globulin, cortisol, thyroid stimulating hormone, triiodothyronine, and thyroxine were obtained. Data were analyzed for correlations and compared against normative reference values. There was a significant positive correlation between TT and cortisol (R
MeSH term(s)	Adult ; Athletes ; Energy Intake ; Humans ; Male ; Middle Aged ; Nutrition Surveys ; Testosterone/blood ; Young Adult
Chemical Substances	Testosterone (3XMK78S47O)
Language	English
Publishing date	2019-10-03
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	80312-1
ISSN	1878-5867 ; 0039-128X
ISSN (online)	1878-5867
ISSN	0039-128X
DOI	10.1016/j.steroids.2019.108504
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Article ; Online: Amelioration of palmitate-induced metabolic dysfunction in L6 muscle cells expressing low levels of receptor-interacting protein 140.

Constantinescu, Silvana / Turcotte, Lorraine P

Canadian journal of physiology and pharmacology

2015 Volume 93, Issue 11, Page(s) 913–922

Abstract: We have shown that reduced expression of receptor-interacting protein 140 (RIP140) alters the regulation of fatty-acid (FA) oxidation in muscle. To determine whether a high level of FA availability alters the effects of RIP140 on metabolic regulation, L6 ...

Abstract	We have shown that reduced expression of receptor-interacting protein 140 (RIP140) alters the regulation of fatty-acid (FA) oxidation in muscle. To determine whether a high level of FA availability alters the effects of RIP140 on metabolic regulation, L6 myotubes were transfected with or without RNA interference oligonucleotide sequences to reduce RIP140 expression, and then incubated with high levels of palmitic acid, with or without insulin. High levels of palmitate reduced basal (53%-58%) and insulin-treated (24%-44%) FA uptake and oxidation, and increased basal glucose uptake (88%). In cells incubated with high levels of palmitate, low RIP140 increased basal FA uptake and insulin-treated FA oxidation and glucose uptake, and decreased basal glucose uptake and insulin-treated FA uptake. Under basal conditions, low RIP140 increased the mRNA content of FAT/CD36 (159%) and COX4 (61%), as well as the protein content of Nur77 (68%), whereas the mRNA expression of FGF21 (50%) was decreased, as was the protein content of CPT1b (35%) and FGF21 (44%). Under insulin-treated conditions, low RIP140 expression increased the mRNA content of MCAD (84%) and Nur77 (84%), as well as the protein content of Nur77 (23%). Thus, a low level of RIP140 restores the rates of FA uptake in the basal state, in part via a reduction in upstream insulin signaling. Our data also indicate that the protein expression of Nur77 may be modulated by RIP140 when muscle cells are metabolically challenged by high levels of palmitate.
MeSH term(s)	Animals ; Cell Line ; Fatty Acids/metabolism ; Gene Expression Regulation ; Muscle Fibers, Skeletal/drug effects ; Muscle Fibers, Skeletal/metabolism ; Myoblasts/drug effects ; Myoblasts/metabolism ; Nuclear Receptor Co-Repressor 1/biosynthesis ; Nuclear Receptor Subfamily 4, Group A, Member 1/biosynthesis ; Palmitic Acid/toxicity ; Rats
Chemical Substances	Fatty Acids ; Nr4a1 protein, rat ; Nuclear Receptor Co-Repressor 1 ; Nuclear Receptor Subfamily 4, Group A, Member 1 ; Palmitic Acid (2V16EO95H1)
Language	English
Publishing date	2015-11
Publishing country	Canada
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	127527-6
ISSN	1205-7541 ; 0008-4212
ISSN (online)	1205-7541
ISSN	0008-4212
DOI	10.1139/cjpp-2015-0020
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Article ; Online: AMPK-α2 is involved in exercise training-induced adaptations in insulin-stimulated metabolism in skeletal muscle following high-fat diet.

Abbott, Marcia J / Turcotte, Lorraine P

Journal of applied physiology (Bethesda, Md. : 1985)

2014 Volume 117, Issue 8, Page(s) 869–879

Abstract: AMP-activated protein kinase (AMPK) has been studied extensively and postulated to be a target for the treatment and/or prevention of metabolic disorders such as insulin resistance. Exercise training has been deemed a beneficial treatment for obesity and ...

Abstract	AMP-activated protein kinase (AMPK) has been studied extensively and postulated to be a target for the treatment and/or prevention of metabolic disorders such as insulin resistance. Exercise training has been deemed a beneficial treatment for obesity and insulin resistance. Furthermore, exercise is a feasible method to combat high-fat diet (HFD)-induced alterations in insulin sensitivity. The purpose of this study was to determine whether AMPK-α2 activity is required to gain beneficial effects of exercise training with high-fat feeding. Wild-type (WT) and AMPK-α2 dominant-negative (DN) male mice were fed standard diet (SD), underwent voluntary wheel running (TR), fed HFD, or trained with HFD (TR + HFD). By week 6, TR, irrespective of genotype, decreased blood glucose and increased citrate synthase activity in both diet groups and decreased insulin levels in HFD groups. Hindlimb perfusions were performed, and, in WT mice with SD, TR increased insulin-mediated palmitate uptake (76.7%) and oxidation (>2-fold). These training-induced changes were not observed in the DN mice. With HFD, TR decreased palmitate oxidation (61-64%) in both WT and DN and increased palmitate uptake (112%) in the WT with no effects on palmitate uptake in the DN. With SD, TR increased ERK1/2 and JNK1/2 phosphorylation, regardless of genotype. With HFD, TR reduced JNK1/2 phosphorylation, regardless of genotype, carnitine palmitoyltransferase 1 expression in WT, and CD36 expression in both DN and WT. These data suggest that low AMPK-α2 signaling disrupts, in part, the exercise training-induced adaptations in insulin-stimulated metabolism in skeletal muscle following HFD.
MeSH term(s)	AMP-Activated Protein Kinases/metabolism ; Adaptation, Physiological/physiology ; Animals ; Blood Glucose/metabolism ; Blood Glucose/physiology ; CD36 Antigens/metabolism ; Carnitine O-Palmitoyltransferase/metabolism ; Citrate (si)-Synthase/metabolism ; Diet, High-Fat/methods ; Hindlimb/metabolism ; Hindlimb/physiology ; Insulin/metabolism ; Insulin Resistance/physiology ; MAP Kinase Signaling System/physiology ; Male ; Mice ; Mice, Inbred C57BL ; Mitogen-Activated Protein Kinase 8/metabolism ; Mitogen-Activated Protein Kinase 9/metabolism ; Muscle, Skeletal/metabolism ; Muscle, Skeletal/physiology ; Obesity/metabolism ; Obesity/pathology ; Oxidation-Reduction ; Palmitates/metabolism ; Phosphorylation/physiology ; Physical Conditioning, Animal/physiology
Chemical Substances	Blood Glucose ; CD36 Antigens ; Insulin ; Palmitates ; Carnitine O-Palmitoyltransferase (EC 2.3.1.21) ; Citrate (si)-Synthase (EC 2.3.3.1) ; Mitogen-Activated Protein Kinase 9 (EC 2.7.1.24) ; AMPK alpha2 subunit, mouse (EC 2.7.11.1) ; Mitogen-Activated Protein Kinase 8 (EC 2.7.11.24) ; AMP-Activated Protein Kinases (EC 2.7.11.31)
Language	English
Publishing date	2014-10-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	219139-8
ISSN	1522-1601 ; 0021-8987 ; 0161-7567 ; 8750-7587
ISSN (online)	1522-1601
ISSN	0021-8987 ; 0161-7567 ; 8750-7587
DOI	10.1152/japplphysiol.01380.2013
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Article ; Online: Post-Stress Fructose and Glucose Ingestion Exhibit Dissociable Behavioral and Physiological Effects.

Conoscenti, Michael A / Williams, Nicole M / Turcotte, Lorraine P / Minor, Thomas R / Fanselow, Michael S

Nutrients

2019 Volume 11, Issue 2

Abstract: An acute traumatic event can lead to lifelong changes in stress susceptibility and result in psychiatric disease such as Post-Traumatic Stress Disorder (PTSD). We have previously shown that access to a concentrated glucose solution for 24 hours beginning ...

Abstract	An acute traumatic event can lead to lifelong changes in stress susceptibility and result in psychiatric disease such as Post-Traumatic Stress Disorder (PTSD). We have previously shown that access to a concentrated glucose solution for 24 hours beginning immediately after trauma decreased stress-related pathology in the learned helplessness model of PTSD and comorbid major depression. The current study sought to investigate the peripheral physiological effects of post-stress glucose consumption. We exposed 128 male Sprague-Dawley rats to inescapable and unpredictable 1-milliamp electric tail shocks or simple restraint in the learned helplessness procedure. Rats in each stress condition had access to a 40% glucose solution, 40% fructose solution, or water. Blood and liver tissue were extracted and processed for assay. We assessed corticosterone, corticosteroid-binding globulin (CBG), glucose, and liver glycogen concentrations at various time points following stress. We found that rats given access to glucose following exposure to traumatic shock showed a transient rise in blood glucose and an increase in liver glycogen repletion compared to those that received water or fructose following exposure to electric shock. We also found that animals given glucose following shock exhibited reduced free corticosterone and increased CBG compared to their water-drinking counterparts. However, this difference was not apparent when glucose was compared to fructose. These data suggest that post-stress glucose prophylaxis is likely not working via modulation of the HPA axis, but rather may provide its benefit by mitigating the metabolic challenges of trauma exposure.
MeSH term(s)	Animals ; Behavior, Animal/physiology ; Blood Glucose/analysis ; Blood Glucose/metabolism ; Corticosterone/blood ; Corticosterone/metabolism ; Disease Models, Animal ; Eating/physiology ; Eating/psychology ; Fructose/metabolism ; Glucose/metabolism ; Helplessness, Learned ; Liver/metabolism ; Liver Glycogen/analysis ; Liver Glycogen/metabolism ; Male ; Rats ; Rats, Sprague-Dawley ; Stress Disorders, Post-Traumatic/metabolism ; Stress Disorders, Post-Traumatic/physiopathology ; Stress Disorders, Post-Traumatic/psychology ; Stress, Psychological/metabolism ; Stress, Psychological/physiopathology ; Stress, Psychological/psychology ; Transcortin/analysis ; Transcortin/metabolism
Chemical Substances	Blood Glucose ; Liver Glycogen ; Fructose (30237-26-4) ; Transcortin (9010-38-2) ; Glucose (IY9XDZ35W2) ; Corticosterone (W980KJ009P)
Language	English
Publishing date	2019-02-09
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2518386-2
ISSN	2072-6643 ; 2072-6643
ISSN (online)	2072-6643
ISSN	2072-6643
DOI	10.3390/nu11020361
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Article ; Online: TNF-α Stress Response Is Reduced Following Load Carriage Training.

Jensen, Andrew E / Niederberger, Brenda / Jaworski, Rebecca / Devaney, Joseph M / Turcotte, Lorraine P / Kelly, Karen R

Military medicine

2018 Volume 184, Issue 1-2, Page(s) e256–e260

MeSH term(s)	Adolescent ; Adult ; Anthropometry/methods ; Biomarkers/analysis ; Biomarkers/blood ; California ; Exercise Test/methods ; Exercise Test/statistics & numerical data ; Humans ; Male ; Military Personnel/statistics & numerical data ; Stress, Psychological/blood ; Stress, Psychological/enzymology ; Stress, Psychological/physiopathology ; Tumor Necrosis Factor-alpha/analysis ; Tumor Necrosis Factor-alpha/blood ; Weight-Bearing/physiology
Chemical Substances	Biomarkers ; Tumor Necrosis Factor-alpha
Language	English
Publishing date	2018-08-21
Publishing country	England
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	391061-1
ISSN	1930-613X ; 0026-4075
ISSN (online)	1930-613X
ISSN	0026-4075
DOI	10.1093/milmed/usy193
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Article ; Online: Contraction-induced signaling: evidence of convergent cascades in the regulation of muscle fatty acid metabolism.

Turcotte, Lorraine P / Abbott, Marcia J

Canadian journal of physiology and pharmacology

2012 Volume 90, Issue 11, Page(s) 1419–1433

Abstract: The regulation of fatty acid utilization during muscle contraction and exercise remains to be fully elucidated. Evidence suggests that the metabolic responses of skeletal muscle induced by the contraction-induced changes in energy demand are mediated by ... ...

Abstract	The regulation of fatty acid utilization during muscle contraction and exercise remains to be fully elucidated. Evidence suggests that the metabolic responses of skeletal muscle induced by the contraction-induced changes in energy demand are mediated by the activation of a multitude of intracellular signaling cascades. This review addresses the roles played by 3 intracellular signaling cascades of interest in the regulation of fatty acid uptake and oxidation in contracting skeletal muscle; namely, the AMP-activated protein kinase (AMPK), calcium/calmodulin-dependent protein kinases (CaMKs), and the extracellular signal-regulated kinase 1 and 2 (ERK1/2) signaling cascades. Data delineating the potential role of AMPK in cross-talk with CaMKII, CaMK kinase (CaMKK), and ERK1/2 are presented. Collectively, data show that in perfused rodent muscle, regulation of fatty acid uptake and oxidation occurs via (i) CaMKII signaling via both AMPK-dependent and -independent cascades, (ii) CaMKK signaling via both AMPK-dependent and -independent cascades, (iii) AMPK signaling in a time- and intensity-dependent manner, and (iv) ERK1/2 signaling in an intensity-dependent manner.
MeSH term(s)	AMP-Activated Protein Kinases/metabolism ; Animals ; Calcium-Calmodulin-Dependent Protein Kinases/metabolism ; Fatty Acids, Nonesterified/metabolism ; Humans ; MAP Kinase Signaling System ; Muscle Contraction ; Muscle, Skeletal/enzymology ; Muscle, Skeletal/metabolism ; Signal Transduction
Chemical Substances	Fatty Acids, Nonesterified ; Calcium-Calmodulin-Dependent Protein Kinases (EC 2.7.11.17) ; AMP-Activated Protein Kinases (EC 2.7.11.31)
Language	English
Publishing date	2012-11
Publishing country	Canada
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	127527-6
ISSN	1205-7541 ; 0008-4212
ISSN (online)	1205-7541
ISSN	0008-4212
DOI	10.1139/y2012-124
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Article ; Online: Genetic downregulation of receptor-interacting protein 140 uncovers the central role of Akt signalling in the regulation of fatty acid oxidation in skeletal muscle cells.

Constantinescu, Silvana / Turcotte, Lorraine P

Experimental physiology

2012 Volume 98, Issue 2, Page(s) 514–525

Abstract: ... Downregulation of RIP140 increased (P < 0.05) basal palmitate uptake (by 20%) and decreased (P < 0.05) basal ... palmitate oxidation (by 38%). In control small interfering RNA-treated cells, insulin increased (P < 0.05 ... glucose (by 31%) and palmitate uptake (by 20%) and decreased (P < 0.05) palmitate oxidation (by 35 ...

Abstract	The role of the nuclear co-repressor receptor-interacting protein 140 (RIP140) in metabolic regulation, gene and protein expression and insulin signalling in skeletal muscle cells remains to be delineated. To study this question, L6 myotubes were treated with or without an RNA interference oligonucleotide sequence to downregulate RIP140 expression and incubated with or without insulin (1 μM). Downregulation of RIP140 increased (P < 0.05) basal palmitate uptake (by 20%) and decreased (P < 0.05) basal palmitate oxidation (by 38%). In control small interfering RNA-treated cells, insulin increased (P < 0.05) glucose (by 31%) and palmitate uptake (by 20%) and decreased (P < 0.05) palmitate oxidation (by 35%). However, in RIP140 small interfering RNA-treated cells, insulin did not affect (P > 0.05) palmitate uptake and increased (P < 0.05) palmitate oxidation (by 79%). In insulin-mediated conditions, downregulation of RIP140 decreased (P < 0.05) Akt(Ser473) and atypical protein kinase C-ζ(Thr403/410) phosphorylation. As expected, downregulation of RIP140 was accompanied by an increase (P < 0.05) in cytochrome c oxidase subunit 4 isoform 1 and peroxisome proliferator-activated receptor receptor γ coactivator-1α mRNA content. Downregulation of RIP140 increased (P < 0.05) fatty acid transport protein 1 mRNA content and carnitine palmitoyltransferase 1b protein content and decreased (P < 0.05) medium chain acyl-CoA dehydrogenase mRNA content in basal conditions. In insulin-mediated conditions, downregulation of RIP140 increased (P < 0.05) carnitine palmitoyltransferase 1b, fatty acid transport protein 1 and fibroblast growth factor 21 mRNA content and decreased (P < 0.05) medium chain acyl-CoA dehydrogenase mRNA content and plasma membrane fatty acid translocase/cluster of differentiation 36 protein content. Our data show that, in skeletal muscle cells, RIP140 expression significantly impacts palmitate uptake and oxidation and that alterations in gene expression and Akt-atypical protein kinaseC-ζ signalling can partly explain these changes.
MeSH term(s)	Acyl-CoA Dehydrogenase/genetics ; Acyl-CoA Dehydrogenase/metabolism ; Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/metabolism ; Animals ; CD36 Antigens/genetics ; CD36 Antigens/metabolism ; Carnitine O-Palmitoyltransferase/genetics ; Carnitine O-Palmitoyltransferase/metabolism ; Cell Line ; Down-Regulation ; Electron Transport Complex IV/metabolism ; Fatty Acid-Binding Proteins/genetics ; Fatty Acid-Binding Proteins/metabolism ; Fibroblast Growth Factors/genetics ; Fibroblast Growth Factors/metabolism ; Glucose/metabolism ; Insulin/metabolism ; Isoenzymes/metabolism ; Muscle Fibers, Skeletal/enzymology ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Nuclear Receptor Interacting Protein 1 ; Oxidation-Reduction ; Palmitic Acid/metabolism ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha ; Phosphorylation ; Protein Kinase C/metabolism ; Protein Kinase C-theta ; Proto-Oncogene Proteins c-akt/metabolism ; RNA Interference ; RNA, Messenger/metabolism ; RNA-Binding Proteins/genetics ; RNA-Binding Proteins/metabolism ; Rats ; Signal Transduction/genetics ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Transfection
Chemical Substances	Adaptor Proteins, Signal Transducing ; CD36 Antigens ; Cd36 protein, rat ; Fabp1 protein, rat ; Fatty Acid-Binding Proteins ; Insulin ; Isoenzymes ; Nuclear Proteins ; Nuclear Receptor Interacting Protein 1 ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha ; Ppargc1a protein, rat ; RNA, Messenger ; RNA-Binding Proteins ; Transcription Factors ; fibroblast growth factor 21 ; Palmitic Acid (2V16EO95H1) ; Fibroblast Growth Factors (62031-54-3) ; Acyl-CoA Dehydrogenase (EC 1.3.8.7) ; Electron Transport Complex IV (EC 1.9.3.1) ; Carnitine O-Palmitoyltransferase (EC 2.3.1.21) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Prkcq protein, rat (EC 2.7.11.13) ; Protein Kinase C (EC 2.7.11.13) ; Protein Kinase C-theta (EC 2.7.11.13) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2012-08-23
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1016295-1
ISSN	1469-445X ; 0958-0670
ISSN (online)	1469-445X
ISSN	0958-0670
DOI	10.1113/expphysiol.2012.068833
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Article ; Online: Effect of voluntary exercise upon the metabolic syndrome and gut microbiome composition in mice.

Moore, Timothy M / Terrazas, Anthony / Strumwasser, Alexander R / Lin, Amanda J / Zhu, Xiaopeng / Anand, Akshay T S / Nguyen, Christina Q / Stiles, Linsey / Norheim, Frode / Lang, Jennifer M / Hui, Simon T / Turcotte, Lorraine P / Zhou, Zhenqi

Physiological reports

2021 Volume 9, Issue 21, Page(s) e15068

Abstract: The metabolic syndrome is a cluster of conditions that increase an individual's risk of developing diseases. Being physically active throughout life is known to reduce the prevalence and onset of some aspects of the metabolic syndrome. Furthermore, ... ...

Abstract	The metabolic syndrome is a cluster of conditions that increase an individual's risk of developing diseases. Being physically active throughout life is known to reduce the prevalence and onset of some aspects of the metabolic syndrome. Furthermore, previous studies have demonstrated that an individual's gut microbiome composition has a large influence on several aspects of the metabolic syndrome. However, the mechanism(s) by which physical activity may improve metabolic health are not well understood. We sought to determine if endurance exercise is sufficient to prevent or ameliorate the development of the metabolic syndrome and its associated diseases. We also analyzed the impact of physical activity under metabolic syndrome progression upon the gut microbiome composition. Utilizing whole-body low-density lipoprotein receptor (LDLR) knockout mice on a "Western Diet," we show that long-term exercise acts favorably upon glucose tolerance, adiposity, and liver lipids. Exercise increased mitochondrial abundance in skeletal muscle but did not reduce liver fibrosis, aortic lesion area, or plasma lipids. Lastly, we observed several changes in gut bacteria and their novel associations with metabolic parameters of clinical importance. Altogether, our results indicate that exercise can ameliorate some aspects of the metabolic syndrome progression and alter the gut microbiome composition.
MeSH term(s)	Adiposity ; Animals ; Gastrointestinal Microbiome ; Glucose/metabolism ; Liver/metabolism ; Male ; Metabolic Syndrome/metabolism ; Metabolic Syndrome/physiopathology ; Metabolic Syndrome/therapy ; Mice ; Mice, Inbred C57BL ; Mitochondria, Liver/metabolism ; Physical Conditioning, Animal/methods ; Receptors, LDL/genetics ; Receptors, LDL/metabolism ; Running
Chemical Substances	Receptors, LDL ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2021-11-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2724325-4
ISSN	2051-817X ; 2051-817X
ISSN (online)	2051-817X
ISSN	2051-817X
DOI	10.14814/phy2.15068
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Article ; Online: HIV protease inhibitors induce metabolic dysfunction in part via increased JNK1/2 pro-inflammatory signaling in L6 cells.

Bogachus, Lindsey D / Turcotte, Lorraine P

Antiviral research

2011 Volume 92, Issue 3, Page(s) 415–423

Abstract: ... uptake (P<0.05) and atazanavir sulfate + ritonavir treatment increased basal glucose uptake significantly ... more than ritonavir or atazanavir sulfate treatment alone (P<0.05). Atazanavir sulfate + ritonavir ... treatment for 48 h completely prevented insulin stimulation of glucose uptake (P>0.05). When compared ...

Abstract	Protease inhibitors (PIs), such as atazanavir sulfate and ritonavir, are used clinically to prevent the progression of HIV and are known to induce insulin resistance. To determine whether PI-mediated insulin resistance is induced by activation of pro-inflammatory cascades, L6 skeletal muscle cells were treated ±atazanavir sulfate, ritonavir, or atazanavir sulfate + ritonavir, and ±insulin. Treatment with atazanavir sulfate, ritonavir, or atazanavir sulfate + ritonavir for 24 or 48 h significantly increased basal glucose uptake (P<0.05) and atazanavir sulfate + ritonavir treatment increased basal glucose uptake significantly more than ritonavir or atazanavir sulfate treatment alone (P<0.05). Atazanavir sulfate + ritonavir treatment for 48 h completely prevented insulin stimulation of glucose uptake (P>0.05). When compared to untreated cells, basal palmitate uptake and oxidation was found to be significantly higher in cells treated with PIs alone or in combination (P<0.05). Prior PI treatment alone or in combination prevented (P>0.05) the insulin-mediated increase in palmitate uptake and the insulin-mediated decrease in palmitate oxidation observed in the control group. Atazanavir sulfate treatment alone or in combination with ritonavir significantly increased JNK1/2 phosphorylation when compared to the control or ritonavir group (P<0.05) and this was accompanied by a rise (P<0.05) in AKT(Ser473) phosphorylation in the basal state. Total JNK1/2 and p38 MAPK protein content and p38 MAPK phosphorylation state were not altered in any of the treatment groups (P>0.05). Our data indicate that, in muscle cells, PIs induce metabolic dysfunction that is not limited to insulin-sensitive metabolism and that is potentially mediated by a rise in JNK1/2 pro-inflammatory signaling.
MeSH term(s)	Animals ; Atazanavir Sulfate ; Cell Line ; Glucose/metabolism ; HIV Protease Inhibitors/pharmacology ; Insulin Resistance ; Mitogen-Activated Protein Kinase 8/metabolism ; Mitogen-Activated Protein Kinase 9/metabolism ; Muscle Fibers, Skeletal/drug effects ; Muscle Fibers, Skeletal/enzymology ; Muscle Fibers, Skeletal/metabolism ; Oligopeptides/pharmacology ; Oxidation-Reduction/drug effects ; Palmitates/metabolism ; Phosphorylation/drug effects ; Proto-Oncogene Proteins c-akt/metabolism ; Pyridines/pharmacology ; Rats ; Ritonavir/pharmacology ; Signal Transduction/drug effects ; Time Factors ; p38 Mitogen-Activated Protein Kinases/metabolism
Chemical Substances	HIV Protease Inhibitors ; Oligopeptides ; Palmitates ; Pyridines ; Atazanavir Sulfate (4MT4VIE29P) ; Mitogen-Activated Protein Kinase 9 (EC 2.7.1.24) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Mitogen-Activated Protein Kinase 8 (EC 2.7.11.24) ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; Glucose (IY9XDZ35W2) ; Ritonavir (O3J8G9O825)
Language	English
Publishing date	2011-12
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	306628-9
ISSN	1872-9096 ; 0166-3542
ISSN (online)	1872-9096
ISSN	0166-3542
DOI	10.1016/j.antiviral.2011.09.008
Database	MEDical Literature Analysis and Retrieval System OnLINE

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