Impaired glucose transport in inguinal adipocytes after short-term high-sucrose feeding in mice

Fryklund, Claes; Borg, Madelene; Svensson, Tobias; Schumacher, Sara; Negoita, Florentina; Morén, Björn; Stenkula, Karin G.

doi:10.1016/j.jnutbio.2019.108338

Cited by 10 publications

(9 citation statements)

References 38 publications

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“…Kampmann et al showed no significant differences in TBC1D4 (and TBC1D1) expression in skeletal muscle among type 2 diabetic patients and matched controls [16]. Short-term high-sucrose diet significantly decreased Tbc1d4 protein expression in murine inguinal and retroperitoneal adipocytes [29], whereas high-fructose diet did not change the total amount of Tbc1d4 protein in murine skeletal muscle [26]. Tbc1d4 expression in murine skeletal muscle was significantly negatively correlated with fasting blood glucose concentration [33], whereas Kristensen et al showed higher expression of TBC1D4 in high glucose presenting porcine adipose and pancreas but not muscle tissue [30].…”

Section: Discussionmentioning

confidence: 98%

“…We have observed no significant effect of adipokines and myokines on both genes expression in cultured human subcutaneous adipocytes. Plethora of methods was used to determine the abundance of TBC1D1 and TBC1D4 on protein and mRNA level, including Western blotting [16,19,20,21,22,23,24,25,12,26,27,28,11,29,14], Reverse Transcription PCR (RT-PCR) [22], quantitative PCR (qPCR) [23,20,30,31,12,26,27,32,28,33,14], microarray [20] and RNA sequencing (RNA-seq) with qPCR validation [34,13,15].…”

Section: Discussionmentioning

confidence: 99%

“…TBC1D4 expression was studied on different mammalian models, including human [24,16,12,34], mouse [20,23,26,27,29,33], rat [22,21,28,11,13,14], mares [19], and pigs [30]. Skeletal muscle was most extensively studied tissue, including muscle biopsy samples as well as cultured myocytes [16,19,20,22,21,24,30,26,27,11,28,13,33], followed by adipose tissue and cultured preadipocytes/adipocytes [16,24,30,23,12,28,29,14]. Type 2 diabetes was shown to decrease expression of Tbc1d4 in skeletal muscle of streptozocin-treated rats [11] and diabetic Goto-Kakizaki rats (in comparison to control Wistar rats) [13].…”

Section: Discussionmentioning

confidence: 99%

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No evidence for change in expression of TBC1D1 and TBC1D4 genes in cultured human adipocytes stimulated by myokines and adipokines

et al. 2021

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TBC1D1 and TBC1D4 proteins play analogous, but not identical role in governing insulin-signalling pathway. Little is known about changes in expression levels of TBC1D1 and TBC1D4 genes in mammals, including humans. Number of factors were studied, but data remain controversial. The aim of this study was to evaluate the effect of selected cytokines, adipokines and myokines with known or putative insulin sensitivity regulation activity (adiponectin, irisin, omentin, interleukin 6, leptin, resistin, and tumour necrosis factor) on TBC1D1 and TBC1D4 expression levels in cultured differentiated human adipocytes. No significant differences were found between the adipocytes treated with different stimuli and this effect was determined not dose dependent. It is reasonable to conclude that relative shortage of data showing no change in TBC1D1 and TBC1D4 from literature results from publication bias; therefore, our finding provides additional insight into the role of both genes.

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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No evidence for change in expression of TBC1D1 and TBC1D4 genes in cultured human adipocytes stimulated by myokines and adipokines

et al. 2021

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“…Short-term overfeeding was carried out as previously described (2, 20, 42). Male C57BL/6J mice (Taconic, Ry, Denmark) were used at 8-9 weeks of age.…”

Section: Methodsmentioning

confidence: 99%

A multi-scale in silico mouse model for insulin resistance and humanoid type 2 diabetes

Simonsson

Bergqvist²,

Gennemark

et al. 2021

Preprint

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Insulin resistance (IR) causes compensatory insulin production, which in humans eventually progresses to beta-cell failure and type 2 diabetes (T2D). This disease progression involves multi-scale processes, ranging from intracellular signaling to organ-organ and whole-body level regulations, on timescales from minutes to years. T2D progression is commonly studied using overfed and genetically modified rodents. However, rodents do not exhibit human T2D progression, with IR-driven beta-cell failure, and available multi-scale data is too complex to fully comprehend using traditional analysis. To help resolve these issues, we here present an in silico mouse model. This is the first mathematical model that simultaneously explains multi-scale mouse IR data on all three levels – cells, organs, body – ranging from minutes to months. The model correctly predicts new independent multi-scale validation data and provides insights into non-measured processes. Finally, we present a humanoid in silico mouse exhibiting disease progression from IR to IR-driven T2D.

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“…The increase in WAT mass associated with sucrose intake might be dependent on excess caloric intake or diet duration (48), because C57BL6J mice fed a sucrose‐enriched diet (3.86 kcal/g, 35% energy from sucrose) did not have increased WAT mass or show increased insulin resistance compared with mice fed an isocaloric diet (3.86 kcal/g, 7% energy from sucrose). However, isolated adipocytes from the inguinal depot of mice fed the sucrose‐enriched diet showed increased size, decreased insulin sensitivity, and decreased expression of the glucose transporter GLUT4 (49). Together, these data suggest that an adiposity‐independent effect of dietary sucrose is to drive insulin resistance and reduce fatty acid breakdown (50) (Figure 1B).…”

Section: Regulation Of Food Intake and Body Weight By Sucrose: Focus ...mentioning

confidence: 99%

Integrating the effects of sucrose intake on the brain and white adipose tissue: Could autophagy be a possible link?

Mattar

Toledo-Valenzuela

Hernández-Cáceres

et al. 2022

Obesity

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Excess dietary sucrose is associated with obesity and metabolic diseases. This relationship is driven by the malfunction of several cell types and tissues critical for the regulation of energy balance, including hypothalamic neurons and white adipose tissue (WAT). However, the mechanisms behind these effects of dietary sucrose are still unclear and might be independent of increased adiposity. Accumulating evidence has indicated that dysregulation of autophagy, a fundamental process for maintenance of cellular homeostasis, alters energy metabolism in hypothalamic neurons and WAT, but whether autophagy could mediate the detrimental effects of dietary sucrose on hypothalamic neurons and WAT that contribute to weight gain is a matter of debate.In this review, we examine the hypothesis that dysregulated autophagy in hypothalamic neurons and WAT is an adiposity-independent effect of sucrose that contributes to increased body weight gain. We propose that excess dietary sucrose leads to autophagy unbalance in hypothalamic neurons and WAT, which increases caloric intake and body weight, favoring the emergence of obesity and metabolic diseases.

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Impaired glucose transport in inguinal adipocytes after short-term high-sucrose feeding in mice

Cited by 10 publications

References 38 publications

No evidence for change in expression of TBC1D1 and TBC1D4 genes in cultured human adipocytes stimulated by myokines and adipokines

No evidence for change in expression of TBC1D1 and TBC1D4 genes in cultured human adipocytes stimulated by myokines and adipokines

A multi-scale in silico mouse model for insulin resistance and humanoid type 2 diabetes

Integrating the effects of sucrose intake on the brain and white adipose tissue: Could autophagy be a possible link?

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