Dietary trans-fat combined with monosodium glutamate induces dyslipidemia and impairs spatial memory

Collison, Kate S.; Makhoul, Nadine J.; Inglis, Angela; Al-Johi, Mohammed; Zaidi, Marya Z.; Maqbool, Zakia; Saleh, Soad; Bakheet, Razan; Mondreal, Rhea; Al-Rabiah, Rana; Shoukri, Mohammed; Milgram, Norton W.; Al‐Mohanna, Futwan

doi:10.1016/j.physbeh.2009.11.010

Cited by 37 publications

(29 citation statements)

References 64 publications

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“…It has been shown, that MSG (120 mg/kg/day) in combination with aspartame elevated body weight and caused 2.3-fold increase in fasting blood glucose compared to standard chow and also caused increased insulin resistance during the Insulin Tolerance Test compared to aspartame alone (50 mg/kg/day), which caused 1.6-fold increase in fasting blood glucose with reduction of insulin sensitivity during an Insulin Tolerance Test in mice (Collison et al 2012). MSG combined with dietary trans-fat increased central adiposity and dyslipidemia compared to mice fed with either trans-fatty acids-enriched diet or dietary MSG alone (Collison et al 2010a).…”

Section: Obesity and Metabolic Disturbancesmentioning

confidence: 86%

Monosodium Glutamate Toxic Effects and Their Implications for Human Intake: A Review

Husarova¹,

Ostatníková²

2013

JMED

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Monosodium Glutamate (MSG) is one of the world's most widely used food additives. Its toxic effects have been shown in numerous animal studies, however in most of them, the method of administration and the doses were not similar to human MSG intake. In this paper we review animal and human studies in which MSG effects on central nervous system, adipose tissue and liver, reproductive organs and other systems have been shown and we discuss their implications for human MSG intake.

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Section: Obesity and Metabolic Disturbancesmentioning

confidence: 86%

Monosodium Glutamate Toxic Effects and Their Implications for Human Intake: A Review

Husarova¹,

Ostatníková²

2013

JMED

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“…hepatic tG quantitation Levels of mouse liver TG were quantified at 32 weeks of age from snap-frozen tissue using the Triglyceride Determination Kit TRO100 with appropriate TG standards (Sigma Aldrich, St Louis, MO) as described previously (8). Briefly, liver samples were first powdered under liquid nitrogen and the lipids extracted with chloroform:methanol (2:1, vol/vol).…”

Section: Materials and Methods Animals And Dietsmentioning

confidence: 99%

“…HFCS and crystalline fructose consumption increases annually, and now accounts for a per capita average of 200 kcal/day (~10% of total calorie intake) (7). We have previously demonstrated that dietary HFCS induces hepatic steatosis and mitochondrial disruption in vitro and in vivo (8); furthermore, HFCS consumption has also been shown to contribute to obesity and impaired insulin sensitivity in a rodent model of NAFLD induced by trans-fat feeding (9). In this clinically relevant model, the investigators established the validity of examining the contribution of several commonly consumed dietary risk factors toward the development of hepatic steatosis.…”

Section: Introductionmentioning

confidence: 99%

Effect of Dietary Monosodium Glutamate on HFCS‐Induced Hepatic Steatosis: Expression Profiles in the Liver and Visceral Fat

Collison

Maqbool

Inglis

et al. 2010

Obesity

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It has previously been shown that patients with nonalcoholic fatty liver disease (NAFLD) exhibit alterations in both hepatic and adipose tissue metabolism, and the dietary factors that contribute to the pathogenesis of NAFLD are likely to be multifactorial. Using C57BL/6J mice, we examined whether chronic exposure to low‐dose dietary monosodium glutamate (MSG), high‐fructose corn syrup (HFCS), or a combination of the two, vs. control would affect metabolism and hepatic and visceral fat gene expression in adult male progeny. A maternal diet containing 20% HFCS and/or dietary MSG (97.2 ± 6.3 mg/kg body weight (bw), provided in the drinking water) was offered ad libitum from 3 weeks before mating, and continued throughout gestation and weaning until the progeny reached 32 weeks of age. Liver and abdominal fat gene expression was compared with control animals fed isocaloric standard chow under identical conditions. HFCS induced hepatic steatosis and increased the expression of genes involved in carbohydrate and lipid metabolism. Conversely, dietary MSG elevated serum free fatty acids (FFAs), triglycerides (TGs), high‐density lipoprotein‐cholesterol (HDL‐C), and insulin, together with the expression of hepatic genes involved in lipid metabolism and bile synthesis. The HFCS+MSG combination elevated hepatic TGs, serum FFAs, and TG levels. In visceral white adipose tissue, both MSG and HFCS diets increased the expression of transcription factor Srebf2 and decreased expression of Ppargc1a, while downregulating the expression of mitochondrial respiratory chain components. MSG increased the expression of several genes implicated in adipocytes differentiation. We hypothesize that HFCS may promote hepatic steatosis, whereas dietary MSG induces dyslipidemia and markers of insulin resistance.

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“…In a study by Phivilay et al (2009), Aβ- and tau-pathology was unaltered in the brain tissue of an AD-mouse model after dietary supplementation of TFAs. Another study reported a declined spatial learning performance of mice fed with a TFA- and monosodium glutamate-rich diet (Collison et al, 2010). …”

Section: The Impact Of Trans Fatty Acids On Admentioning

confidence: 99%

APP Function and Lipids: A Bidirectional Link

Grimm

Mett

Grimm

et al. 2017

Front. Mol. Neurosci.

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Extracellular neuritic plaques, composed of aggregated amyloid-β (Aβ) peptides, are one of the major histopathological hallmarks of Alzheimer’s disease (AD), a progressive, irreversible neurodegenerative disorder and the most common cause of dementia in the elderly. One of the most prominent risk factor for sporadic AD, carrying one or two aberrant copies of the apolipoprotein E (ApoE) ε4 alleles, closely links AD to lipids. Further, several lipid classes and fatty acids have been reported to be changed in the brain of AD-affected individuals. Interestingly, the observed lipid changes in the brain seem not only to be a consequence of the disease but also modulate Aβ generation. In line with these observations, protective lipids being able to decrease Aβ generation and also potential negative lipids in respect to AD were identified. Mechanistically, Aβ peptides are generated by sequential proteolytic processing of the amyloid precursor protein (APP) by β- and γ-secretase. The α-secretase appears to compete with β-secretase for the initial cleavage of APP, preventing Aβ production. All APP-cleaving secretases as well as APP are transmembrane proteins, further illustrating the impact of lipids on Aβ generation. Beside the pathological impact of Aβ, accumulating evidence suggests that Aβ and the APP intracellular domain (AICD) play an important role in regulating lipid homeostasis, either by direct effects or by affecting gene expression or protein stability of enzymes involved in the de novo synthesis of different lipid classes. This review summarizes the current literature addressing the complex bidirectional link between lipids and AD and APP processing including lipid alterations found in AD post mortem brains, lipids that alter APP processing and the physiological functions of Aβ and AICD in the regulation of several lipid metabolism pathways.

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Dietary trans-fat combined with monosodium glutamate induces dyslipidemia and impairs spatial memory

Cited by 37 publications

References 64 publications

Monosodium Glutamate Toxic Effects and Their Implications for Human Intake: A Review

Monosodium Glutamate Toxic Effects and Their Implications for Human Intake: A Review

Effect of Dietary Monosodium Glutamate on HFCS‐Induced Hepatic Steatosis: Expression Profiles in the Liver and Visceral Fat

APP Function and Lipids: A Bidirectional Link

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