Is insulin resistance tissue-dependent and substrate-specific? The role of white adipose tissue and skeletal muscle

Calderón-DuPont, Diana; Torre‐Villalvazo, Ivan; Dı́az-Villaseñor, Andrea

doi:10.1016/j.biochi.2022.08.021

Cited by 8 publications

(8 citation statements)

References 235 publications

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“…In addition, ceramide, a lipid component constituting the cell membrane and usually synthesized from palmitic acid, is produced by TNFα activated sphingomyelinase [ 186 ]. Ceramide activates protein phosphatase 2 (PP2) to dephosphorylate Akt and activates JNK1 and IKKβ and induces serine phosphorylation of IRS1 & 2 which weakens the intracellular insulin signaling [ 187 ].…”

Section: Insulin and Insulin Resistancementioning

confidence: 99%

How Can Insulin Resistance Cause Alzheimer’s Disease?

Yoon

Hwang

Son

et al. 2023

IJMS

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Alzheimer’s disease (AD) is a neurodegenerative disorder associated with cognitive decline. Despite worldwide efforts to find a cure, no proper treatment has been developed yet, and the only effective countermeasure is to prevent the disease progression by early diagnosis. The reason why new drug candidates fail to show therapeutic effects in clinical studies may be due to misunderstanding the cause of AD. Regarding the cause of AD, the most widely known is the amyloid cascade hypothesis, in which the deposition of amyloid beta and hyperphosphorylated tau is the cause. However, many new hypotheses were suggested. Among them, based on preclinical and clinical evidence supporting a connection between AD and diabetes, insulin resistance has been pointed out as an important factor in the development of AD. Therefore, by reviewing the pathophysiological background of brain metabolic insufficiency and insulin insufficiency leading to AD pathology, we will discuss how can insulin resistance cause AD.

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Section: Insulin and Insulin Resistancementioning

confidence: 99%

How Can Insulin Resistance Cause Alzheimer’s Disease?

Yoon

Hwang

Son

et al. 2023

IJMS

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“…During 24 h of monitoring, eugenol increased respiratory exchange rates and energy metabolism in T2DM mice and significantly increased exercise levels at night. Skeletal muscles are an important organ for insulin action, and insulin resistance results in reduced glucose uptake, decreased exercise capacity, and eventually skeletal muscle atrophy ( 32 , 33 ). It has been reported that 35% of glucose is absorbed by muscles and produces energy ( 34 ).…”

Section: Discussionmentioning

confidence: 99%

Eugenol improves high-fat diet/streptomycin-induced type 2 diabetes mellitus (T2DM) mice muscle dysfunction by alleviating inflammation and increasing muscle glucose uptake

et al. 2022

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Eugenol has been used in dietary interventions for metabolic diseases such as diabetes and obesity. However, the protective effect of eugenol on muscle function in diabetes is unclear. In this study, a high-fat diet (HFD) with a streptozocin (STZ) injection induced type II diabetes mellitus in a mouse model. Oral eugenol lowered blood glucose and insulin resistance of HFD/STZ-treated mice. Eugenol reduced HFD/STZ-induced muscle inflammation and prevented muscle weakness and atrophy. Eugenol administration significantly increased GLUT4 translocation and AMPK phosphorylation in skeletal muscle, thereby enhancing glucose uptake. By silencing the transient receptor potential vanilloid channel 1 (TRPV1) gene in C2C12 myotube cells, eugenol was found to increase intracellular Ca2+ levels through TRPV1, which then activated calmodulin-dependent protein kinase-2 (CaMKK2) and affected AMPK protein phosphorylation. In conclusion, eugenol is a potential nutraceutical for preventing high-glucose-induced muscle impairments, which could be explained by its mediating effects on glucose absorption and inflammatory responses in the muscle.

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“…Adipose tissue expansion and subsequent insulin resistance-induced hyperglycaemia is considered the key driver of sterile metabolic inflammation in T2DM patients. The link between visceral adipose tissue (VAT) dysfunction and insulin resistance is well established (Calderón-DuPont et al 2022, Kahn et al 2022. Dysregulated expansion and hypertrophy of VAT during obesity induce tissue hypoxia; alter the secretory profile of adipokines, cytokines/chemokines, and bioactive lipids; and modify the distribution and quantity of immune cells within the tissue (Fig.…”

Section: Mechanisms Underlying Chronic Metabolic Inflammationmentioning

confidence: 99%

Section: Mechanisms Underlying Chronic Metabolic Inflammationmentioning

confidence: 99%

“…There is thus an accumulation of extracellular glucose (hyperglycaemia) in circulation, whereas intracellular glucose availability for glycerol and fatty acid synthesis is reduced due to insulin resistance. This leads to a further reduction in lipogenesis (esterification and synthesis of signalling bioactive lipids) within adipose tissue, whilst the impaired antilipolytic effects of insulin result in an increase in circulating free fatty acids(Calderón- DuPont et al 2022). Together this leads to glucotoxicity and lipotoxicity inducing a myriad of complications related to multisystem cellular senescence and organ failure.Prolonged hyperglycaemia causes glucose to form covalent bonds with various plasma proteins (albumin, fibrinogen, globulins, collagen), intracellular lipids, and nucleic acids to form different types of advanced glycation end products (AGEs) that interfere with the normal function of these molecules(Singh et al 2014).…”

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confidence: 99%

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Immunology of chronic low-grade inflammation: relationship with metabolic function

Vyver

2023

Journal of Endocrinology

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Inflammation is part of the body’s innate immune response and is an essential process that not only defends against harmful bacteria and pathogens but also plays a key role in the maintenance and repair of tissues. Under pathological conditions, there is bilateral crosstalk between immune regulation and aberrant metabolism resulting in persistent inflammation in the absence of infection. This phenomenon is referred to as sterile metabolic inflammation (metainflammation) and occurs if the initiating stimulus is not removed or if the resolution process is disrupted. Disruption of this tightly regulated immune response and its failure to resolve as is evident in metabolic disorders and is not only associated with disease progression but also leads to immune senescence and should not be neglected in the clinical management of patients. This review gives an overview of the mechanisms underlying chronic metabolic inflammation, the aberrant metabolic activation of innate immune cells (neutrophils, macrophages, mast cells, dendritic cells) and its role in disease progression using obesity-diabetes as a prime example. Addressing the underlying subclinical metabolic inflammation in addition to achieving glucose control may contribute significantly towards therapeutic interventions aimed at preventing the onset of co-morbidities in diabetic patients.

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Is insulin resistance tissue-dependent and substrate-specific? The role of white adipose tissue and skeletal muscle

Cited by 8 publications

References 235 publications

How Can Insulin Resistance Cause Alzheimer’s Disease?

How Can Insulin Resistance Cause Alzheimer’s Disease?

Eugenol improves high-fat diet/streptomycin-induced type 2 diabetes mellitus (T2DM) mice muscle dysfunction by alleviating inflammation and increasing muscle glucose uptake

Immunology of chronic low-grade inflammation: relationship with metabolic function

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