Fructose increases corticosterone production in association with NADPH metabolism alterations in rat epididymal white adipose tissue

Prince, Paula D.; Santander, Yanina; Gerez, Esther Noemí; Höcht, Christián; Polizio, Ariel Héctor; Mayer, Marc; Taira, Carlos A.; Fraga, César G.; Galleano, Mónica; Carranza, Andrea

doi:10.1016/j.jnutbio.2017.02.021

Cited by 15 publications

(17 citation statements)

References 55 publications

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“…In accordance with this, an increase of corticosterone in WAT and plasma accompanied total WAT gain in rats fed with 10% fructose (w/v) in drinking water [53]. The authors also reported that this finding was due to the high activity/expression of H6PDH and 11β-HSD1 in epididymal WAT [53]. In vitro studies of fructose-induced adipogenesis in 3T3-L1 cells showed an increase in 11β-HSD1 expression, which promoted high endogenous GC levels [12].…”

Section: Fructose Induces Adipogenesis By Gc Actionmentioning

confidence: 62%

“…Fructose consumption increases active GC levels through 11β-HSD1 activity in rat WAT [52]. In accordance with this, an increase of corticosterone in WAT and plasma accompanied total WAT gain in rats fed with 10% fructose (w/v) in drinking water [53]. The authors also reported that this finding was due to the high activity/expression of H6PDH and 11β-HSD1 in epididymal WAT [53].…”

Section: Fructose Induces Adipogenesis By Gc Actionmentioning

confidence: 85%

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High Fructose Intake and Adipogenesis

Hernández-Díazcouder

Romero‐Nava

Carbó

et al. 2019

IJMS

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In modern societies, high fructose intake from sugar-sweetened beverages has contributed to obesity development. In the diet, sucrose and high fructose corn syrup are the main sources of fructose and can be metabolized in the intestine and transported into the systemic circulation. The liver can metabolize around 70% of fructose intake, while the remaining is metabolized by other tissues. Several tissues including adipose tissue express the main fructose transporter GLUT5. In vivo, chronic fructose intake promotes white adipose tissue accumulation through activating adipogenesis. In vitro experiments have also demonstrated that fructose alone induces adipogenesis by several mechanisms, including (1) triglycerides and very-low-density lipoprotein (VLDL) production by fructose metabolism, (2) the stimulation of glucocorticoid activation by increasing 11β-HSD1 activity, and (3) the promotion of reactive oxygen species (ROS) production through uric acid, NOX and XOR expression, mTORC1 signaling and Ang II induction. Moreover, it has been observed that fructose induces adipogenesis through increased ACE2 expression, which promotes high Ang-(1-7) levels, and through the inhibition of the thermogenic program by regulating Sirt1 and UCP1. Finally, microRNAs may also be involved in regulating adipogenesis in high fructose intake conditions. In this paper, we propose further directions for research in fructose participation in adipogenesis.

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Section: Fructose Induces Adipogenesis By Gc Actionmentioning

confidence: 62%

Section: Fructose Induces Adipogenesis By Gc Actionmentioning

confidence: 85%

High Fructose Intake and Adipogenesis

Hernández-Díazcouder

Romero‐Nava

Carbó

et al. 2019

IJMS

View full text Add to dashboard Cite

show abstract

“…However, since most fructose is converted to glucose within the liver, high-fructose diets still have the ability to raise blood glucose and stimulate insulin secretion (40). Furthermore, diets with a high percentage of fructose have found to promote significant metabolic alterations (41–44).…”

Section: Fructose Consumptionmentioning

confidence: 99%

Dietary Fructose Consumption and Triple-Negative Breast Cancer Incidence

Strober

Brady

2019

Front. Endocrinol.

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In the past century the western world has found a way to combat most communicative diseases; however, throughout that time the prevalence of obesity, hyperglycemia, and hyperlipidemia have drastically increased. These symptoms characterize metabolic syndrome—a non-communicable disease which has become one of the greatest health hazards of the world. During this same time period the western diet had dramatically changed. Homecooked meals have been replaced by highly-processed, calorically dense foods. This conversion to the current western diet was highlighted by the incorporation of high-fructose corn syrup (HFCS) into sweetened beverages and foods. The consumption of large amounts of dietary sugar, and fructose in particular, has been associated with an altered metabolic state, both systemically and in specific tissues. This altered metabolic state has many profound effects and is associated with many diseases, including diabetes, cardiovascular disease, and even cancer ( 1 ). Specific types of cancer, like triple-negative breast cancer (TNBC), are both responsive to dietary factors and exceptionally difficult to treat, illustrating the possibility for preventative care through dietary intervention in at risk populations. To treat these non-communicable diseases, including obesity, diabetes, and cancer, it is imperative to understand systemic and localized metabolic abnormalities that drive its progression. This review will specifically explore the links between increased dietary fructose consumption, development of metabolic disturbances and increased incidence of TNBC.

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“…A series of serine kinases, including ERK, c-JNK and p38 MAPK [39] can sense lipid metabolites, and inflammatory cytokines in adipocytes and skeletal muscle cells, the activation of which under TNF-α further disturbs the functions of local tissues and organs [139]. IL-6 negatively affects insulin signaling to increase glucose uptake in skeletal muscle and suppress glucose production in liver [140]. The possible mechanism may involve the activation of serine-threonine protein kinase (LKB)1/AMPK/AS160 and JNK-mediated suppression of IRS-1 phosphorylation in skeletal muscle [140].…”

Section: Inflammatory Cytokinesmentioning

confidence: 99%

“…IL-6 negatively affects insulin signaling to increase glucose uptake in skeletal muscle and suppress glucose production in liver [140]. The possible mechanism may involve the activation of serine-threonine protein kinase (LKB)1/AMPK/AS160 and JNK-mediated suppression of IRS-1 phosphorylation in skeletal muscle [140]. High fructose diet induces insulin resistance in skeletal muscle, with nuclear translocation of NF-κB 65, and subsequent secretion of IL-6, which is known to be mostly released from skeletal muscle [141].…”

Section: Inflammatory Cytokinesmentioning

confidence: 99%

Dietary Fructose and Glucose: The Multifacetted Aspects of Their Metabolism and Implication for Human Health

2018

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Fructose increases corticosterone production in association with NADPH metabolism alterations in rat epididymal white adipose tissue

Cited by 15 publications

References 55 publications

High Fructose Intake and Adipogenesis

High Fructose Intake and Adipogenesis

Dietary Fructose Consumption and Triple-Negative Breast Cancer Incidence

Dietary Fructose and Glucose: The Multifacetted Aspects of Their Metabolism and Implication for Human Health

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