Glucocorticoid-induced insulin resistance is related to macrophage visceral adipose tissue infiltration

Huong, Thi Thu; Garcia, Manon; Dalle, H.; Dorothée, Guillaume; Moldes, Marthe; Fève, Bruno; Buyse, Marion

doi:10.1016/j.jsbmb.2018.08.010

Cited by 30 publications

(26 citation statements)

References 57 publications

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“…Indeed, GC-mediated attenuation of acute lung injury in mice was associated with reduced numbers of classical but increased numbers of alternatively activated macrophages in the lungs (78). Similarly, long-term treatment of mice with GCs was associated with increased infiltration of macrophages with an anti-inflammatory phenotype in adipose tissues (142).…”

Section: Gc Effects On Monocyte Adhesion and Migrationmentioning

confidence: 99%

More Than Suppression: Glucocorticoid Action on Monocytes and Macrophages

2019

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Uncontrolled inflammation is a leading cause of many clinically relevant diseases. Current therapeutic strategies focus mainly on immunosuppression rather than on the mechanisms of inflammatory resolution. Glucocorticoids (GCs) are still the most widely used anti-inflammatory drugs. GCs affect most immune cells but there is growing evidence for cell type specific mechanisms. Different subtypes of monocytes and macrophages play a pivotal role both in generation as well as resolution of inflammation. Activation of these cells by microbial products or endogenous danger signals results in production of pro-inflammatory mediators and initiation of an inflammatory response. GCs efficiently inhibit these processes by down-regulating pro-inflammatory mediators from macrophages and monocytes. On the other hand, GCs act on “naïve” monocytes and macrophages and induce anti-inflammatory mediators and differentiation of anti-inflammatory phenotypes. GC-induced anti-inflammatory monocytes have an increased ability to migrate toward inflammatory stimuli. They remove endo- and exogenous danger signals by an increased phagocytic capacity, produce anti-inflammatory mediators and limit T-cell activation. Thus, GCs limit amplification of inflammation by repressing pro-inflammatory macrophage activation and additionally induce anti-inflammatory monocyte and macrophage populations actively promoting resolution of inflammation. Further investigation of these mechanisms should lead to the development of novel therapeutic strategies to modulate undesirable inflammation with fewer side effects via induction of inflammatory resolution rather than non-specific immunosuppression.

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Section: Gc Effects On Monocyte Adhesion and Migrationmentioning

confidence: 99%

More Than Suppression: Glucocorticoid Action on Monocytes and Macrophages

2019

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“…For example, in Cushing’s syndrome, hypercortisolemia increases intraabdominal and subcutaneous fat mass [46,47]. Thus, chronic GC treatments induce weight gain and WAT expansion [48]. It has been long recognized that obesity and obesogenic factors increase endogenous GCs.…”

Section: Fructose Induces Adipogenesis By Gc Actionmentioning

confidence: 99%

High Fructose Intake and Adipogenesis

Hernández-Díazcouder

Romero‐Nava

Carbó

et al. 2019

IJMS

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In modern societies, high fructose intake from sugar-sweetened beverages has contributed to obesity development. In the diet, sucrose and high fructose corn syrup are the main sources of fructose and can be metabolized in the intestine and transported into the systemic circulation. The liver can metabolize around 70% of fructose intake, while the remaining is metabolized by other tissues. Several tissues including adipose tissue express the main fructose transporter GLUT5. In vivo, chronic fructose intake promotes white adipose tissue accumulation through activating adipogenesis. In vitro experiments have also demonstrated that fructose alone induces adipogenesis by several mechanisms, including (1) triglycerides and very-low-density lipoprotein (VLDL) production by fructose metabolism, (2) the stimulation of glucocorticoid activation by increasing 11β-HSD1 activity, and (3) the promotion of reactive oxygen species (ROS) production through uric acid, NOX and XOR expression, mTORC1 signaling and Ang II induction. Moreover, it has been observed that fructose induces adipogenesis through increased ACE2 expression, which promotes high Ang-(1-7) levels, and through the inhibition of the thermogenic program by regulating Sirt1 and UCP1. Finally, microRNAs may also be involved in regulating adipogenesis in high fructose intake conditions. In this paper, we propose further directions for research in fructose participation in adipogenesis.

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“…Furthermore, the influence of ACTH and GCs on food intake, weight gain, and fat metabolism confounds the use of weight as an indicator of overall health. Prolonged exposure to increased GC levels can result in weight gain (Scerif et al, 2013 ; Do et al, 2019 ). However, the GC-induced weight gain may require a dosage regimen extending further than 7-days, as used in our study, as previous work has shown that 1 week of increased GC levels did not result in increased body weight (Do et al, 2019 ).…”

Section: Discussionmentioning

confidence: 99%

“…Prolonged exposure to increased GC levels can result in weight gain (Scerif et al, 2013 ; Do et al, 2019 ). However, the GC-induced weight gain may require a dosage regimen extending further than 7-days, as used in our study, as previous work has shown that 1 week of increased GC levels did not result in increased body weight (Do et al, 2019 ). Furthermore, several studies have demonstrated that central administration of ACTH results in reduced food intake (Al-Barazanji et al, 2001 ; Schulz et al, 2010 ; Shipp et al, 2015 ) and weight loss compared to the vehicle when given ad libitum access to food (Al-Barazanji et al, 2001 ).…”

Section: Discussionmentioning

confidence: 99%

Cosyntropin Attenuates Neuroinflammation in a Mouse Model of Traumatic Brain Injury

Siebold

Krueger

Abdala

et al. 2020

Front. Mol. Neurosci.

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Aim : Traumatic brain injury (TBI) is a leading cause of mortality/morbidity and is associated with chronic neuroinflammation. Melanocortin receptor agonists including adrenocorticotropic hormone (ACTH) ameliorate inflammation and provide a novel therapeutic approach. We examined the effect of long-acting cosyntropin (CoSyn), a synthetic ACTH analog, on the early inflammatory response and functional outcome following experimental TBI. Methods : The controlled cortical impact model was used to induce TBI in mice. Mice were assigned to injury and treatment protocols resulting in four experimental groups including sham + saline, sham + CoSyn, TBI + saline, and TBI + CoSyn. Treatment was administered subcutaneously 3 h post-injury and daily injections were given for up to 7 days post-injury. The early inflammatory response was evaluated at 3 days post-injury through the evaluation of cytokine expression (IL1β and TNFα) and immune cell response. Quantification of immune cell response included cell counts of microglia/macrophages (Iba1+ cells) and neutrophils (MPO+ cells) in the cortex and hippocampus. Behavioral testing ( n = 10–14 animals/group) included open field (OF) and novel object recognition (NOR) during the first week following injury and Morris water maze (MWM) at 10–15 days post-injury. Results : Immune cell quantification showed decreased accumulation of Iba1+ cells in the perilesional cortex and CA1 region of the hippocampus for CoSyn-treated TBI animals compared to saline-treated. Reduced numbers of MPO+ cells were also found in the perilesional cortex and hippocampus in CoSyn treated TBI mice compared to their saline-treated counterparts. Furthermore, CoSyn treatment reduced IL1β expression in the cortex of TBI mice. Behavioral testing showed a treatment effect of CoSyn for NOR with CoSyn increasing the discrimination ratio in both TBI and Sham groups, indicating increased memory performance. CoSyn also decreased latency to find platform during the early training period of the MWM when comparing CoSyn to saline-treated TBI mice suggesting moderate improvements in spatial memory following CoSyn treatment. Conclusion : Reduced microglia/macrophage accumulation and neutrophil infiltration in conjunction with moderate improvements in spatial learning in our CoSyn treated TBI mice suggests a beneficial anti-inflammatory effect of CoSyn following TBI.

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Glucocorticoid-induced insulin resistance is related to macrophage visceral adipose tissue infiltration

Cited by 30 publications

References 57 publications

More Than Suppression: Glucocorticoid Action on Monocytes and Macrophages

More Than Suppression: Glucocorticoid Action on Monocytes and Macrophages

High Fructose Intake and Adipogenesis

Cosyntropin Attenuates Neuroinflammation in a Mouse Model of Traumatic Brain Injury

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