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20 November 2025

A Systematic Review of Palmitate-Mediated Insulin Resistance in C2C12 Myotubes

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Department of Health and Human Performance, High Point University, High Point, NC 27268, USA
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Nutrients2025, 17(22), 3619;https://doi.org/10.3390/nu17223619
This article belongs to the Section Nutrition and Diabetes
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Abstract

Background/Objectives: Skeletal muscle plays a pivotal role in whole-body glucose metabolism and is a major target in the pathogenesis and treatment of insulin resistance and type 2 diabetes. The C2C12 myotube cell line is one of the most used in vitro models to investigate mechanisms of insulin resistance. This systematic review (1) summarizes the most common experimental conditions including palmitate concentrations and treatment durations used to induce insulin resistance in C2C12 myotubes; (2) characterizes outcomes related to insulin resistance; and (3) discusses strengths and limitations associated with this model. Methods: A systematic search of PubMed and Scopus was conducted using terms “C2C12 AND palmitate AND insulin resistance” and related variations. A total of 191 articles met inclusion criteria. Results: The most frequently used palmitate concentrations were 0.25 mM, 0.5 mM, and 0.75 mM for at least 16 h, which consistently led to decreased insulin-stimulated pAkt expression, GLUT4 abundance, and insulin-stimulated glucose uptake. Conclusions: The high volume and consistency of primary findings is a key strength of this article which demonstrated reduced insulin signaling across various culture conditions, treatment durations, and insulin co-stimulation protocols.

1. Introduction

Skeletal muscle is a metabolically important and active contributor to human movement and physiology. Skeletal muscle is also a consequential tissue for several pathologies such as insulin resistance and diabetes, due to its key role in glucose metabolism. For this reason, skeletal muscle is a primary target tissue for improving insulin sensitivity for the benefit of metabolic disease. Thus, exploring the mechanisms of insulin resistance in skeletal muscle is noble and offers the possibility of treatments. Among the most common experimental proof-of-concept strategies is the use of in vitro systems such as the myoblast cell culture line, C2C12. Originally, C2C12 cells were isolated from mouse skeletal muscle and can differentiate into multinucleated myotubes. Moreover, it is known to be insulin-responsive and is recognized as a convenient and effective model for studying several attributes of muscle physiology during health and disease including insulin resistance [].
While there are other methods of inducing insulin resistance in vitro, treatment of cultured myotubes with the saturated fatty acid, specifically palmitate, is among the most widely used. A prodigious number of primary research articles have utilized this technique for inducing insulin resistance, and many of these manuscripts have focused on methods of restoring the palmitate-mediated reduction in insulin signaling. Given the widespread use of palmitate-treated myotubes as a model of insulin resistance, and because of how common the palmitate-treated C2C12 myotube model has become, there is a need to summarize the common features of this model. Therefore, this systematic review was undertaken to provide a summary of common features of palmitate-mediated insulin resistance in C2C12 myotubes.

1.1. Mechanistic Overview of Palmitate-Mediated Insulin Resistance

In general, several mechanisms have been proposed for how palmitate promotes insulin resistance, much of which has been described elsewhere [,]. Briefly, the accumulation of various lipid subtypes in skeletal muscle may disrupt several signaling cascades; observations which date back to 1999 []. For example, increased lipid accumulation including ceramides, diacylglycerols, and other lipids can activate inflammatory signaling such as I kappa B kinase (Iκκ) (directly by lipid excess or via increased protein kinase c (PKC)). PKC and Iκκ activation can ultimately inhibit insulin receptor substrate 1 (IRS1), thereby reducing cell responsiveness to insulin stimulation. Reduced IRS1 response to insulin stimulation results in reductions in Akt activation, glucose transporter 4 (GLUT4) abundance, and GLUT4 translocation to the cell membrane. Additionally, lipid toxicity is also associated with increased reactive oxygen species production, which is associated with organelle dysfunction, especially mitochondrial dysfunction. Collectively, reduced response within the canonical insulin signaling pathway, reduced mitochondrial function, and heightened reactive oxygen species (ROS) are all common features of palmitate-mediated insulin resistance in C2C12 myotubes (Figure 1). Detailed mechanistic overviews of lipid mediated insulin resistance are available at the following reviews [,].
Figure 1. Mechanistic overview of palmitate-induced insulin resistance. Notes: Solid black arrows denote signaling and activation. Arrows that travel behind a molecular target indicate that the molecular target over the arrow phosphorylates the target from which arrow originates. Green arrows indicate normal insulin signaling mechanisms. Red arrows indicate the contribution of this pathway negatively impacts insulin signaling. Dashed arrows indicate the uptake of palmitate or translocation of GLUT4 vesicles. Abbreviations: GLUT4, glucose transporter member 4; GSV, GLUT4 storage vesicles; Iκκ, I kappa B kinase; IRS1, insulin receptor substrate 1; IR, insulin receptor; PI3K, phosphatidylinositol 3-kinase; PKC, protein kinase c; ROS, reactive oxygen species; TLR4, toll-like receptor 4.

1.2. Aims and Scope of Review

Given the increasing prevalence of insulin resistance and diabetes, experiments that assess basic attributes and mechanisms for potential therapeutics are important. Because palmitate-mediated insulin resistance in C2C12 myotubes is a commonly used model for assessing insulin resistance, this work aims to (1) highlight the concentrations and durations commonly used in palmitate-mediated insulin resistance in C2C12 myotubes; (2) describe the effects of palmitate-mediated insulin resistance in C2C12 myotubes on various outcomes associated with both basal and insulin signaling response; and (3) discuss the current obstacles and considerations associated with this model. In general, the most frequently used palmitate concentrations were 0.25 mM, 0.5 mM, and 0.75 mM for at least 16 h, which consistently led to decreased insulin-stimulated pAkt expression, GLUT4 abundance, and insulin-stimulated glucose uptake. Obstacles such as highly variable culture conditions, insulin stimulation protocol, use of far beyond pharmacokinetically attainable levels of palmitate and loss of cell viability are among the most prominent obstacles in the use of palmitate-treated C2C12 myotubes as a model for skeletal muscle insulin resistance. Importantly, multiple other in vitro models and cell lines are also commonly used but not included (such as L6 or Primary Human Skeletal Muscle Cells (HSkMC)). However, C2C12 myotubes were focused on in the present report because it is among the most used model of mimicking skeletal muscle in vitro.

2. Materials and Methods

2.1. General Article Search Procedure and Eligibility Criteria

Primary literature was identified by RAV first by searching PubMed and Scopus using individual “C2C12 AND palmitate AND insulin resistance”. The search was then repeated with “palmitate” substituted with “palmitic acid” both with the addition of each targeted outcome (for example “pAkt”) both with and without the presence of “insulin resistance”. Initially, full texts for each article were screened by RAV (as the abstract is insufficient in many cases to know if eligible experiments were contained within the manuscript). Articles were included and summarized if (1) C2C12 myotubes were used as the cell culture model of insulin resistance, (2) the article included a palmitate-only group along with appropriate vehicle or true control, (3) the article assessed at least one of the related outcomes associated with the canonical insulin signaling pathway of importance to the scope of the review (per PRISMA guidelines, the outcomes are included as column topics within each table). Additionally, when appropriate, experiments with modified C2C12 cell line (i.e., reporter, siRNA, etc.) were included if relevant comparisons and outcomes were included with corresponding control.

2.2. Secondary Article Screening and Inclusion Procedure

All references were initially screened for eligibility by a single reviewer (RAV) with curation completed using the publication date of 19 June 2025 (and final article curation completed as of 8 October 2025). Articles which were initially excluded were then reassessed for eligibility criteria by a second independent author (JMZ), and incorrectly omitted articles were also included and summarized. Articles that were deemed eligible following initial screening were then re-evaluated by a second independent member of the research team (JMZ, AJK, and KBT), at which point measurements/estimates of effects for each outcome were made. Estimates of outcomes were generated using ratio-metric measurements of palmitate treatment versus relevant control (or raw data was reported when available). Importantly, although quality control and risk of bias is essential to guarantee the scientific quality of each individual study, standards of reporting for in vitro experiments have changed substantially since the introduction of the model. Moreover, limited risk-of-bias assessment tools are validated for in vitro studies (specifically related to the presented outcomes), therefore a bias assessment was not performed for each report.
Additionally, because the concentrations of palmitate used in the literature varied widely (from 0.05–1.2 mM), we stratified the results from each included paper into 3 tiers of concentrations. These tiers are (1) those that used pharmacokinetically attainable levels which include concentrations ≤0.25 mM, (2) those that used palmitate concentrations that moderately exceed pharmacokinetically attainable levels ranging from 0.251–0.5 mM, and (3) those which well-exceed pharmacokinetic levels (proof-of-concept), which include treatment conditions >0.5 mM palmitate. The determination of pharmacokinetically attainable concentrations was based on observations showing levels of palmitate approximate 0.007–0.015 mM (fasting []) up to 0.145–0.210 mM (post-prandial []). Additionally, to provide a summary of the most relevant treatment conditions, a general estimate of the effect of the most common concentration and treatment duration was summarized in text for each outcome as the average relative values of palmitate treatments versus control (control = 100) following variable insulin stimulation conditions (presented as total experimental average ± SD versus relative control). Importantly, these estimated average effects do not include data for protein expression only quantified by visual confirmation (VC). Additionally, within some individual studies, multiple distinct experiments were conducted involving differing treatment conditions (such as varying treatment duration) and are therefore provided as independent rows within each Table.

3. Results

3.1. Search Results

An initial historical search identified an article published as early as 1999 which first assessed the effect of palmitate conjugated with BSA on insulin signaling in C2C12 cells []. Initial search results from both PubMed and Scopus identified 1325 search results. After removing duplicate articles from overlapping search results, a total of 310 articles were identified and twice-screened (initially by RAV and secondarily by a separate independent author for verification of inclusion criteria and generation of estimated effect). After further removal of articles without relevant experimental conditions and/or outcomes, unavailable texts, review articles, articles not in English, and retractions, a total of 191 articles were included (Figure 2). Further details regarding article inclusion/exclusion results (Supplementary Table S1) and raw data estimates (Supplementary File S1) are provided within the Supplemental Materials.
Figure 2. Flowchart of search strategy and results from PubMed and Scopus search. Search strategy for palmitate-mediated insulin resistance in C2C12 myotubes using “C2C12 AND palmitate AND insulin resistance” with and without targets related to insulin resistance as outlined in Methods and figure above.

3.2. Organization of Data

We examined the effect of palmitate at various concentrations on insulin signaling in C2C12 myotubes, analyzing changes in phosphorylated IRS (pIRS), phosphorylated Akt (pAkt), GLUT4, and glucose uptake under both basal and insulin-stimulated states. As noted above, under normal conditions, insulin binds to its receptor and activates IRS via phosphorylation. Downstream, this activates Akt through phosphorylation, which promotes GLUT4 translocation to the cell membrane to ultimately promote glucose uptake. Therefore, to reveal the effect of palmitate on insulin signaling, we highlight the response of myotubes following insulin stimulation, which reveals the effect on responsiveness to insulin. Though, for reference and completeness, we also include the results from basal experiments within each Table. Also as noted above, because the concentrations of palmitate used in the literature varied widely (from 0.05–1.2 mM), we have stratified the results into 3 tiers of concentrations including those that approximate pharmacokinetically attainable levels which include concentrations ≤0.25 mM (Table 1). These concentrations were chosen based on observations demonstrating levels of palmitate approximate 0.007–0.015 mM (fasting []) up to 0.145–0.210 mM (post-prandial []). Additionally, other experiments were stratified as those that used palmitate concentrations that moderately exceed pharmacokinetically attainable levels ranging from 0.251–0.5 mM (Table 2), and those which well-exceeded pharmacokinetic (proof-of-concept) levels including treatment conditions >0.5 mM (Table 3). Moreover, to provide a summary of the most relevant treatment conditions, a general estimate of the effect of the most common concentration and treatment duration was summarized in text for each outcome as the average relative values of palmitate treatments versus control (control = 100%) following variable insulin stimulation conditions (presented as average ± SD). Importantly, these estimated average effects do not include data for protein expression only quantified by VC.
Table 1. Findings from systematic search results on the effect of pharmacokinetically attainable levels of palmitate treatment at various concentrations for various durations on common indicators of insulin sensitivity.
Table 2. Findings from systematic search results on the effect of moderately greater than pharmacokinetically attainable levels of palmitate treatment at various concentrations for various durations on common indicators of insulin sensitivity.
Table 3. Findings from systematic search results on the effect of far greater than pharmacokinetically attainable (proof-of-concept) levels of palmitate treatment at various concentrations for various durations on common indicators of insulin sensitivity.

3.3. Effect of Pharmacokinetically Attainable Levels of Palmitate on Insulin Signaling

We began by assessing the reported effects of pharmacokinetically attainable palmitate levels (concentrations ≤ 0.25 mM), which accounted for about 1/3 of the experimental observations, on common indicators of insulin sensitivity. Expression of pAkt following insulin stimulation was the most common measurement of the inclusion criteria outcomes. Within the experiments that utilized pharmacokinetically attainable levels, 0.2 mM for 24 h was the most common set of treatment conditions. Cells treated with 0.2 mM for 24 h exhibited decreased pIRS expression (total experimental average 37.9 ± 17.0% versus control following variable insulin stimulation). Similar reductions in pAkt expression, GLUT4, and glucose uptake were observed following treatment with 0.2 mM for 24 h (total experimental average for pAkt (43.1 ± 23.2%), GLUT4 (70.0 ± 19.9%), and glucose uptake (56.0 ± 19.3%), following variable insulin stimulation conditions). Additional experimental results for all included articles that utilized treatments with pharmacokinetically attainable levels of palmitate are included in Table 1.

3.4. Effect of Moderately Higher than Pharmacokinetically Attainable Levels of Palmitate on Insulin Signaling

Next, we continued summarizing the effect of palmitate on insulin sensitivity by assessing the reported effect of experiments that utilized moderately higher than pharmacokinetically attainable levels (concentrations 0.251–0.5 mM), which, again accounted for about 1/3 of the experimental observations. Consistent with findings from Table 1, expression of pAkt following insulin stimulation was again the most common measurement of the inclusion criteria outcomes. Within the experiments that utilized moderately higher than pharmacokinetically attainable levels, 0.5 mM for 16 h was the most common set of treatment conditions. Following treatment with 0.5 mM for 16 h, the palmitate-treated cells exhibited mixed effects on pIRS expression (total experimental average 136.4 ± 69.0% versus control following variable insulin stimulation). However, like pharmacokinetically attainable levels of palmitate, 0.5 mM palmitate consistently reduced pAkt expression (57.6 ± 21.5%), GLUT4 (48.0 ± 22.2%), and glucose uptake (61.5 ± 23.8%), following variable insulin stimulation conditions. Additional experimental results for all included articles that utilized treatments with moderately higher than pharmacokinetically attainable levels of palmitate are included in Table 2.

3.5. Effect of “Proof-of-Concept” Levels of Palmitate on Insulin Signaling

Lastly, we completed summarizing the effect of palmitate on insulin sensitivity by assessing the reported effect of experiments that utilized concentrations of palmitate that are far higher than pharmacokinetically attainable levels or “proof-of-concept” levels (concentrations > 0.5 mM), which accounted for roughly the final 1/3 of the experimental observations. Once again, expression of pAkt following insulin stimulation remained the most observed measurement of the inclusion criteria outcomes. Within the experiments that utilized proof-of-concept levels, 0.75 mM for 16 h was the most common set of treatment conditions. Unlike moderately high levels of palmitate, treatment with 0.75 mM palmitate for 16 h displayed relatively consistent reductions in pIRS expression (total experimental average 68.9 ± 71.8% versus control following variable insulin stimulation). Moreover, treatment with 0.75 mM palmitate for 16 h also consistently reduced pAkt expression (50.1 ± 14.6%), GLUT4 (55.3 ± 39.6%), and glucose uptake (61.0 ± 24.7%), following variable insulin stimulation conditions. Additional experimental results for all included articles that utilized proof-of-concept levels of palmitate treatments are described in Table 3.

4. Discussion

The present systematic review examined 191 published studies that investigated palmitate-induced insulin resistance in C2C12 myotubes. In general, the most frequently used palmitate concentrations were 0.25 mM, 0.5 mM, and 0.75 mM for at least 16 h, which consistently led to decreased insulin-stimulated pAkt expression, GLUT4 abundance, and insulin-stimulated glucose uptake. Within this review, we placed an emphasis on the most common treatment conditions for each level of palmitate treatment used within experiments. Collectively, the results from the studies reveal well-conserved effects of palmitate exposure on insulin signaling and glucose uptake.

4.1. IRS

IRS activation following insulin stimulation is considered a component of the proximal canonical insulin signaling pathway []. The most inconsistent finding of our review was the effect of palmitate treatment on IRS activation following insulin stimulation. Of the most common treatment conditions at pharmacokinetically attainable palmitate levels, pIRS expression was consistently reduced. Conversely, experiments that utilized moderately higher than pharmacokinetically attainable palmitate levels exhibited mixed results. However, proof-of-concept concentrations which far exceed the pharmacokinetically attainable palmitate levels of palmitate found reduced IRS activation following insulin stimulation. Such disparities may be due to a concentration-dependent effect during which, at low levels, palmitate impedes the action of insulin signaling in the mechanism outlined in Figure 1. However, at levels moderately higher than those which are pharmacokinetically attainable, palmitate may activate IRS via mTORC-dependent mechanisms which can further reduce insulin sensitivity []. Finally, at proof-of-concept concentrations, palmitate again reduces the activation of IRS possibly due to off-target mechanisms (such as reduced cell viability, discussed below). Thus, additional dose-dependent studies should investigate the importance of timing and concentration of palmitate treatment to elucidate if the disparate findings across concentrations are due to experimental variability, or the speculated hypothesis outlined above involving both concentration-dependent effects confounded by cytotoxicity.

4.2. Akt

Unlike IRS, Akt activation following insulin stimulation was the most common measurement and most consistent finding in the present review. In fact, consistently reduced pAkt expression following insulin stimulation was observed across all levels of palmitate treatment. That said, like IRS, Akt activation is considered a component of the proximal canonical insulin signaling pathway. As such, it has been discussed that under some experimental circumstances, large changes in Akt activation may not necessarily equate to large changes in the activation/inactivation of downstream targets, and that loss of Akt activation alone may not explain the entirety of the status of insulin resistance []. This ‘spareness’ exhibited by Akt and other proximal signaling molecules implies that only small amounts of function of such signals may be required to elicit the physiological response.

4.3. GLUT4

Unlike IRS and Akt activation, which are components of the proximal canonical insulin signaling pathway, GLUT4 vesicle translocation to the plasma membrane does not exhibit the same ‘spareness’ as IRS and Akt activation and is therefore less debated on its importance during insulin resistance. Thus, an important finding within this report is that GLUT4 levels were consistently reduced in the most common treatment conditions from all three categories of palmitate concentrations. However, an important limitation of these measurements was that several reports did not assess membrane translocation. That said, of the reports that assessed both GLUT4 levels and glucose uptake, it appears that when GLUT4 levels were reduced, so were levels of glucose uptake.

4.4. Glucose Uptake

The final indicator of insulin sensitivity assessed in the current report is the uptake of glucose, which is not a portion of signaling cascade, but rather the mechanistic outcome of the functional cascade. Like Akt activation and GLUT4 levels, glucose uptake was consistently reduced across all three levels of palmitate treatment. And as noted above, a striking consistency between GLUT4 abundance and glucose uptake was observed across most reports that assessed both outcomes. However, important disparities across reports are worthy of consideration. For example, the duration of fasting (serum, glucose, or both) and composition of media components (high versus low glucose) both before and during the insulin stimulation experiments. Similarly, the duration of and concentration of insulin treatment also varied substantially between reports.

4.5. Limitations and Considerations

In general, the collective results from the summarized experiments align with impaired insulin signaling and are consistent with the mechanisms of lipid-induced insulin resistance, including the hypothesis that excess saturated fatty acids disrupt insulin receptor substrate (IRS1) signaling, impair phosphatidylinositol 3-kinase (PI3K)/Akt pathway activity, and reduce downstream glucose uptake [,]. However, it is acknowledged that the multifaceted nature of lipid toxicity in skeletal muscle (such as its capacity to promote inflammation, impair other signaling cascades, and disrupt metabolic homeostasis) are other topics worthy of comment. Therefore, a limitation of the current review is the selective scope which included only the effect of palmitate treatment on insulin signaling and glucose uptake. Future comments on the effect of palmitate treatment on markers of inflammation and metabolic dysfunction are warranted.
Additionally, several limitations are worth noting. First, the preparation and conjugation of palmitate to bovine serum albumin (BSA) is a critical step in ensuring bioavailability and reducing toxicity. This step varied across the studies, resulting in a lack of standardization. This methodological variability could influence both the magnitude and reproducibility of the observed effects. Secondly, the duration and concentration of insulin stimulation used to assess insulin responsiveness varied widely, making direct comparisons across independent studies more complex. Thirdly, C2C12 myotubes differ from primary human skeletal muscle (in vitro and in vivo) in several keyways. Moreover, the in vitro C2C12 model lacks interplay with other tissues and can only serve as a simplified model in this context. Thus, while the C2C12 myotubes are useful for insight regarding the mechanisms, findings from this model may not provide full insight into the physiological mechanisms and responses noted in human tissue. And finally, a major limitation worthy of considering is the common use of palmitate levels that far exceed pharmacokinetically attainable levels. This is important as the physiological relevance of these findings for in vivo systems is questionable. Moreover, several reports noted loss of cell viability at several of the utilized concentrations (most commonly >0.3 mM). In fact, several reports noted loss of cell viability (usually assessed via tetrazolium assay) at pharmacokinetically attainable levels [,,,,,], though it was more common for these lower concentrations to not affect viability. However, these observations raise questions about the off-target mechanisms of palmitate concentrations that exceeded these levels.

4.6. Strengths and Conclusions

Despite the limitations highlighted above, our review has several strengths. First, a strength of this report is the volume and consistency of the primary findings. The reliability of reduced insulin signaling following palmitate treatment despite differences in culture conditions, treatment durations, and insulin co-stimulation protocols across various studies demonstrates a high degree of reproducibility of the model. Indeed, reductions in insulin-stimulated pAkt and GLUT4 levels as well as consistently reduced insulin-stimulated glucose uptake provide convincing evidence of the reliability in palmitate-treated myotubes as a model of skeletal muscle insulin resistance. These shared features across studies emphasize and reinforce the validity and utility of the palmitate–C2C12 model as a robust in vitro system for probing mechanisms related to insulin resistance.
Collectively, this report demonstrates the highly consistent dose- and time-dependent effects of palmitate-mediated insulin resistance in the C2C12 myotube model of skeletal muscle. The findings herein may also be useful by informing future studies of in vitro models of insulin resistance and serve as a user’s reference for C2C12 myotube insulin resistance.

Supplementary Materials

The following supporting information can be downloaded at: https://www.mdpi.com/article/10.3390/nu17223619/s1, Table S1: Composite search results and inclusion/exclusion results from Pubmed and Scopus.; File S1: Raw data estimates of original research [,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,].

Author Contributions

Conceptualization, R.A.V.; methodology, R.A.V.; investigation, J.M.Z., A.J.K., K.B.T., and R.A.V.; resources, R.A.V.; data curation, R.A.V.; writing—original draft preparation, J.M.Z., A.J.K., K.B.T., and R.A.V.; writing—review and editing, J.M.Z., A.J.K., K.B.T., and R.A.V.; visualization, R.A.V.; supervision, R.A.V.; project administration, R.A.V.; funding acquisition, R.A.V. All authors have read and agreed to the published version of the manuscript.

Funding

This work was supported by the Department of Health and Human Performance within the Congdon School of Health Sciences. Additional support was provided by the Congdon School of Health Sciences Summer Undergraduate Research Fellowship (SURF).

Institutional Review Board Statement

Not applicable.

Data Availability Statement

No new data were created or analyzed in this study.

Acknowledgments

The authors have reviewed and edited the output and take full responsibility for the content of this publication. All authors have read and approved the final manuscript.

Conflicts of Interest

The authors declare no conflicts of interest.

Abbreviations

The following abbreviations are used in this manuscript:
3D3 dimensional
Glut4glucose transporter member 4
GSVglut4 storage vesicles
HGhigh glucose
IκκI kappa B kinase
IRS1insulin receptor substrate 1 (protein)
IRinsulin receptor (protein)
LGlow glucose
PI3Kphosphatidylinositol 3-Kinase (protein)
PAktphosphorylated Akt
PKCprotein kinase c
ROSreactive oxygen species
SDstandard deviation
SEMstandard error of the mean
TLR4toll-like receptor 4
VCvisual confirmation

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Design and Validation of the Index of Adherence to the Dietary Guidelines for Chile 2022 (GABAS-Index 17)
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