Skeletal Muscle Nucleo-Mitochondrial Crosstalk in Obesity and Type 2 Diabetes.

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pioglitazone 1 endocrinologydiseasesdrugs
rosiglitazone 1 endocrinologydiseasesdrugs
Insulin 2 endocrinologydiseasesdrugs
glucose intolerance 1 endocrinologydiseases
obesity 33 endocrinologydiseases

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Insulin 13527 can be of significance in various physiological and pathophysiological states.3. HFD-Induced Obesity, Insulin Resistance and Anterograde CommunicationHFD feeding results in differential effects on mitochondrial
Insulin 28598 lipid deposition and attenuate or prevent insulin resistance during obesity.4. HFD-Induced Obesity, Insulin Resistance, and Retrograde CommunicationHFD feeding resulting in obesity and insulin resistance leads
pioglitazone 27597 enhance insulin sensitivity in peripheral tissues [[134]], and synthetic PPAR-ɣ agonists, such as pioglitazone and rosiglitazone, are approved by the FDA for treatment of T2D [[134]]. Muscle specific deletion of
rosiglitazone 27614 sensitivity in peripheral tissues [[134]], and synthetic PPAR-ɣ agonists, such as pioglitazone and rosiglitazone , are approved by the FDA for treatment of T2D [[134]]. Muscle specific deletion of Ppar-γ in mice leads
Select Disease Character Offset Disease Term Instance
glucose intolerance 33935 to acylcarnitines [[155]], leads to increased amounts long chain acylcarnitines in association with glucose intolerance [[153]]. Conversely, when incomplete beta oxidation and accumulation of acylcarnitines in the mitochondrial
obesity 746 may contribute to ectopic lipid deposition and insulin resistance during high fat diet (HFD)-induced obesity . The present review discusses the roles of anterograde and retrograde communication in nucleo-mitochondrial
obesity 1008 mitochondrial adaptations, specifically alterations in mitochondrial number and function in relation to obesity and insulin resistance. Special emphasis is placed on the effects of high fat diet (HFD) feeding on
obesity 1353 receptor gamma coactivator 1 alpha (PGC-1α) in the onset and progression of insulin resistance during obesity and how HFD-induced alterations in NEMG expression affect skeletal muscle mitochondrial adaptations
obesity 2135 excess caloric intake, and consumption of high fat diets (HFD) contribute to metabolic disorders such as obesity , T2D, diabetic dyslipidemia, and non-alcoholic fatty liver disease [[3],[4],[5]]. On the other hand,
obesity 2384 reduction of fat intake and increasing physical activity have been shown to decrease the incidence of obesity and T2D [[6],[7]]. In the absence of positive lifestyle modifications, obese subjects are at a higher
obesity 3031 mechanisms that may contribute to the development and progression of metabolic disorders including obesity and T2D, as well as their complications [[11],[12],[13],[14],[15],[16],[17],[18]]. For example, fatty
obesity 3368 carnitine palmitoyltransferase 1 (CPT-1) and citrate synthase (CS), are lower in the skeletal muscle during obesity , and higher intramyocellular lipid (IMCL) content is observed in insulin resistant subjects [[18],[19]].
obesity 4183 biogenesis and function [[22]] and may play a role in the development of insulin resistance during obesity and T2D [[23],[24]]. Here, we discuss the role of NEMGs in regulating mitochondrial adaptations in the
obesity 4337 of NEMGs in regulating mitochondrial adaptations in the skeletal muscle in relation to HFD-induced obesity and insulin resistance.2. Nucleo-Mitochondrial CrosstalkMitochondria play a significant role in determining
obesity 14211 to prevent insulin resistance or act in other conditions in which increased lipid is present (i.e., obesity ) or during repeated stimulation with HFD to inhibit and/or desensitize FAO and lead to fatty acid accumulation
obesity 15586 chain enzymes in Wistar rats [[79]].Other studies support the conclusion that HFD feeding leads to obesity and insulin resistance, with decreased NEMG expression, impaired mitochondrial function and decreased
obesity 17051 mitochondria, and may play a significant role in determining mitochondrial adaptations that contribute to obesity and insulin resistance. The roles of the NEMGs, NRF-1, NRF-2, PGC-1α, and others in determining mitochondrial
obesity 17237 others in determining mitochondrial number and function in regards to FAO and their potential roles in obesity and insulin resistance are further discussed below.3.1. NRF-1 and NRF-2NRF-1 and NRF-2 are transcription
obesity 19009 T2D [[93]]. Decreased skeletal muscle Nrf-1 and Nrf-2 expression have been noted during HFD-induced obesity [[94]], and Nrf-1 is downregulated in T2D subjects compared to non-diabetic subjects [[93]]. NRF-1 dependent
obesity 25329 contribute to ectopic lipid accumulation and insulin resistance [[82],[119]]. In the skeletal muscle during obesity and insulin resistance, an accumulation of medium and long chain fatty acids has been noted and may
obesity 25506 fatty acids has been noted and may contribute to the onset and progression of insulin resistance during obesity [[120]]. Pgc-1α may attenuate insulin resistance by increasing the completeness of fatty acid beta-oxidation
obesity 25881 in the skeletal muscle [[119]]. Furthermore, Pgc-1α expression is reduced in patients with T2D and obesity , and this reduction seems to be one of the factors responsible for the development and progression of
obesity 26382 [[124],[125],[126],[127]]. These studies point to the fact that PGC-1α is involved in the development of obesity and T2D. Lower Pgc-1α levels that are commonly seen in obese and T2D patients could lead to progression
obesity 26765 in determining mitochondrial number and function [[128]]. Most notable among these with respect to obesity and insulin resistance (in addition to those previously discussed), which are also coactivated by PGC-1α,
obesity 28566 which may act to prevent ectopic lipid deposition and attenuate or prevent insulin resistance during obesity .4. HFD-Induced Obesity, Insulin Resistance, and Retrograde CommunicationHFD feeding resulting in obesity
obesity 28671 obesity.4. HFD-Induced Obesity, Insulin Resistance, and Retrograde CommunicationHFD feeding resulting in obesity and insulin resistance leads to mitochondrial dysfunction that is partially evidenced by incomplete
obesity 28906 acids and ectopic lipid deposition [[76],[82],[119]]. Specifically in the skeletal muscle, HFD-induced obesity is associated with the accumulation of FAO intermediates in the form of long and medium chain acylcarnitines
obesity 29356 of insulin resistance in the skeletal muscle [[140]]. While diets high in dietary fat content induce obesity and insulin resistance in association with incomplete FAO [[76],[82],[119]], dietary supplementation
obesity 30157 formation, transport, and localization of acylcarnitines, and the role of acylcarnitines in HFD-induced obesity and T2D.4.1. Mitochondrial Transport of Intracellular Fatty Acids for OxidationMitochondrial beta oxidation
obesity 32899 acylcarnitines, indicating incomplete beta oxidation of fatty acids, is observed during HFD-induced obesity and insulin resistance [[82]].4.3. Role of Acylcarnitines in Obesity and T2DVarious studies have shown
obesity 33297 diabetic rats, long chain acylcarnitines are increased in the skeletal muscle [[82]]. Human subjects with obesity and T2D also show acylcarnitine accumulation and incomplete beta oxidation in the skeletal muscle [[119],[140]].
obesity 33468 beta oxidation in the skeletal muscle [[119],[140]]. When primary myocytes obtained from subjects with obesity were cultured with lipolytically active adipocytes, medium- and long-chain acylcarnitines accumulated
obesity 35294 throughout the cell, they may play a role in retrograde communication to determine NEMG expression, obesity and insulin resistance [[22],[62],[76],[157]]. Interestingly, in a study by Aguer et al., myocytes treated
obesity 36882 short chain acylcarnitines from the mitochondria may play a contributory role in the development of obesity and insulin resistance in the skeletal muscle through retrograde communication to regulate NEMG expression
obesity 37128 adaptations.5. ConclusionsDecreased NEMG expression and low mitochondrial number and dysfunction are observed in obesity and T2D [[18],[19],[21],[121],[122],[123]]. Based on the literature discussed in this review, it can
obesity 37808 responsible for progressive loss of mitochondrial function and development of insulin resistance seen in obesity and T2D.Figure 1Mitochondrial adaptations, such as alterations in number and function, are determined
obesity 38847 this retrograde communication. Interestingly, in response to high fat diet (HFD) feeding and during obesity and insulin resistance, a downregulation in NEMG expression is seen. Alterations in acylcarnitine profiles
obesity 39423 contribute to increased intramyocellular lipid (IMCL) accumulation and insulin resistance during HFD-induced obesity (left).ijms-18-00831-t001_Table 1Table 1Effects of dietary fat interventions or lipid treatment on skeletal

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