Lysophosphatidic Acid Signaling in Obesity and Insulin Resistance.

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Insulin 4 endocrinologydiseasesdrugs
glucose intolerance 2 endocrinologydiseases
obesity 39 endocrinologydiseases
rosiglitazone 1 endocrinologydiseasesdrugs

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Insulin 63 Title: NutrientsLysophosphatidic Acid Signaling in Obesity and Insulin ResistanceKenneth D’SouzaGeena V. ParamelPetra C. KienesbergerDepartment of Biochemistry and Molecular
Insulin 26387 adiposity can be reversed or ameliorated by ATX-LPA modulation.4. Relationship between ATX-LPA and Insulin Signaling/ResistanceThe ATX–LPA axis is not only implicated in obesity, but may play an important
Insulin 30954 individual LPA receptors in this process.Potential Mechanisms by which the ATX–LPA Axis Influences Insulin ResistanceObesity is characterized by chronic low levels of systemic and tissue inflammation [[80]].
Insulin 40055 transcription factors involve the ATX–LPA axis.5. The ATX–LPA Axis—A Potential Link between Obesity/ Insulin Resistance and Cardiovascular DiseaseObesity and insulin resistance are well-established risk factors
rosiglitazone 38561 involve several tissues [[104]]. Interestingly, treatment of 3T3-L1 and 3T3-F442A adipocytes with the TZD rosiglitazone decreases ATX mRNA, protein content, and secreted ATX activity, suggesting that PPARγ inhibits ATX-LPA
Select Disease Character Offset Disease Term Instance
glucose intolerance 30571 was not examined [[78]]. Taken together, most studies suggest that ATX-LPA-LPA1/3 signaling promotes glucose intolerance and impairs systemic insulin sensitivity and tissue insulin signaling. Future studies should clarify
glucose intolerance 48337 on adipocyte proliferation and differentiation, diet-induced obesity, insulin resistance (IR), and glucose intolerance (GI).Effect of ATX and/or LPA on:ModelsRef.Preadipocyte proliferationPreadipocyte differentiationDiet-induced
obesity 874 (ATX) expression and activity, have been implicated in metabolic and inflammatory disorders including obesity , insulin resistance, and cardiovascular disease. This review summarizes our current understanding of
obesity 1129 on the influence of diet on circulating LPA. Furthermore, we explore how the ATX-LPA pathway impacts obesity and obesity-associated disorders, including impaired glucose homeostasis, insulin resistance, and cardiovascular
obesity 1141 influence of diet on circulating LPA. Furthermore, we explore how the ATX-LPA pathway impacts obesity and obesity -associated disorders, including impaired glucose homeostasis, insulin resistance, and cardiovascular
obesity 2925 pathophysiological conditions, including cancer, arthritis, pulmonary fibrosis, neurological disorders, and obesity -induced insulin resistance and impaired glucose homeostasis [[7],[10],[11],[12],[13],[14],[15]].Under
obesity 16951 LPA levels is through the upregulation of ATX. Prior studies using mice with high-fat diet-induced obesity show increased ATX mRNA and protein expression in adipose tissue, a major source of circulating ATX
obesity 17574 experimental conditions are evident. Therefore, future studies need to clarify precisely how diet-induced obesity is linked to changes in ATX-LPA.3. ATX-LPA Signaling in ObesityIn humans, the relationship between ATX-LPA
obesity 17693 to changes in ATX-LPA.3. ATX-LPA Signaling in ObesityIn humans, the relationship between ATX-LPA and obesity also remains somewhat unclear. In severely obese women (BMI 35.0–64.5), serum ATX does not correlate
obesity 17820 somewhat unclear. In severely obese women (BMI 35.0–64.5), serum ATX does not correlate with markers of obesity , including weight, BMI, or waist circumference [[66]]. However, ATX mRNA is significantly increased
obesity 18649 normalized to sex and the study population consists almost exclusively of individuals with normal BMI or pre obesity , with less than 1% individuals being obese based on BMI [[31]]. Overall, evidence to date suggests that
obesity 18856 that tissue ATX expression and circulating ATX-LPA levels may not correlate well with parameters of obesity across different study populations. Our understanding of the relationship between the ATX-LPA pathway
obesity 18970 different study populations. Our understanding of the relationship between the ATX-LPA pathway and obesity can be improved by examining circulating LPA levels in human cohorts, in addition to ATX expression
obesity 19233 mRNA levels of distinct LPA receptors in insulin sensitive mouse and human tissues are associated with obesity . For example, LPA4, LPA5, and/or LPA6 are significantly increased in myocardial tissue and cells from
obesity 19376 LPA6 are significantly increased in myocardial tissue and cells from HFHS-fed mice and humans with pre obesity or obesity [[16]]. These data suggest that changes in tissue LPA receptor expression may also contribute
obesity 19387 significantly increased in myocardial tissue and cells from HFHS-fed mice and humans with preobesity or obesity [[16]]. These data suggest that changes in tissue LPA receptor expression may also contribute to alterations
obesity 19532 changes in tissue LPA receptor expression may also contribute to alterations in ATX-LPA signaling during obesity .3.1. Role of the ATX–LPA Axis in Preadipocyte Proliferation and DifferentiationAdipocyte hyperplasia
obesity 19733 hyperplasia and hypertrophy are two mechanisms by which adipose tissue expands during development and obesity [[70]]. Through autocrine and paracrine signaling, the ATX–LPA axis is believed to influence both
obesity 19928 influence both processes and play a key role in altering adipose tissue biology and metabolism during obesity . The effect of ATX-LPA signaling on adipose tissue was examined predominantly using preadipocyte models
obesity 24937 heterozygous and adipose-specific ATX deficiencies protect mice on a C57Bl6 background from diet-induced obesity , while adipose-specific ATX overexpression driven from the FABP4 promoter enhances adiposity following
obesity 25109 promoter enhances adiposity following high-fat diet feeding [[31]]. The resistance to diet-induced obesity in FATX−/− mice was ascribed to improved BAT function, lipid oxidation capacity, and energy expenditure
obesity 25871 contributed to these, in part, divergent results among studies examining the role of ATX-LPA in diet-induced obesity [[30],[31],[57],[75]]. Clearly, more research is needed to address the precise role of ATX-LPA signaling
obesity 26000 [[30],[31],[57],[75]]. Clearly, more research is needed to address the precise role of ATX-LPA signaling in diet-induced obesity . Future studies should employ ATX/LPA receptor inhibition/deletion in adult mice before and after the
obesity 26123 should employ ATX/LPA receptor inhibition/deletion in adult mice before and after the induction of obesity , to determine whether the ATX-LPA pathway impacts adiposity independent of its possible effect on preadipocyte
obesity 26460 Relationship between ATX-LPA and Insulin Signaling/ResistanceThe ATX–LPA axis is not only implicated in obesity , but may play an important role in the regulation of glucose homeostasis and insulin sensitivity. Subjecting
obesity 28574 homeostasis and insulin resistance, and that ATX-LPA may serve as a therapeutic target and/or marker for obesity -related insulin resistance in humans.While a relationship between ATX-LPA and systemic glucose homeostasis
obesity 31244 factor α (TNFα), are elevated systemically and locally within the adipose tissue of murine models of obesity and diabetes, and contribute directly to obesity-induced insulin resistance [[81]]. TNFα neutralization
obesity 31293 locally within the adipose tissue of murine models of obesity and diabetes, and contribute directly to obesity -induced insulin resistance [[81]]. TNFα neutralization improves peripheral insulin sensitivity in these
obesity 31584 resistance [[81]]. In addition to TNFα, several other pro-inflammatory cytokines are increased in obesity and contribute to the development and/or exacerbation of insulin resistance, including monocyte chemoattractant
obesity 35306 3).Altered energy homeostasis, signified by greater intake than expenditure of calories, is a hallmark of obesity and obesity-induced insulin resistance. BAT thermogenesis through respiration uncoupling plays a key
obesity 35318 homeostasis, signified by greater intake than expenditure of calories, is a hallmark of obesity and obesity -induced insulin resistance. BAT thermogenesis through respiration uncoupling plays a key role in regulating
obesity 35582 [[90],[91],[92],[93],[94]]. Studies on humans demonstrate an inverse relationship between BAT activity and obesity /BMI [[95],[96],[97]]. In line with this notion, increasing BAT activity through cold acclimatization
obesity 36886 biogenesis in white adipose tissue [[75]]. Interestingly, while these mice show increased diet-induced obesity , glucose homeostasis is unchanged [[75]]. In HFD-fed FATX−/− mice, improved insulin sensitivity
obesity 39271 circulating adiponectin [[30],[31]]. Notably, circulating adiponectin is inversely correlated with obesity and insulin resistance, and has insulin sensitizing effects on skeletal muscle and liver [[108],[109],[110],[111],[112]].
obesity 39685 proteins in insulin-resistant adipocytes [[55]]. Taken together, the ATX-LPA pathway may contribute to obesity -induced insulin resistance by impairing PPARγ expression and activity (Figure 3). The mechanism by
obesity 40540 that changes in the ATX-LPA pathway play an important role in promoting cardiovascular disease during obesity /insulin resistance. LPA levels are significantly higher in coronary arteries harboring atherosclerotic
obesity 45086 to be tested if and to what extent the ATX–LPA axis impacts cardiovascular disease associated with obesity , insulin resistance, and diabetes, and whether LPA signaling influences cardiomyopathy and heart failure
obesity 45369 clearly implicated the ATX-LPA-LPA1-6 signaling axis in the development of metabolic disorders, including obesity , insulin resistance, and impaired glucose homeostasis, as well as cardiovascular disease. Targeting
obesity 47099 nature. Future studies should test the potential of ATX and LPA receptor modulators for the treatment of obesity - and diabetes-related metabolic disease and other comorbidities.Figure 1Metabolism of circulating lysophosphatidic
obesity 47994 promotes insulin resistance and impaired glucose homeostasis. The ATX-LPA pathway may contribute to obesity -induced insulin resistance by stimulating inflammation and fibrosis and/or suppressing brown adipose
obesity 48299 1Table 1The influence of ATX-LPA signaling on adipocyte proliferation and differentiation, diet-induced obesity , insulin resistance (IR), and glucose intolerance (GI).Effect of ATX and/or LPA on:ModelsRef.Preadipocyte

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