Hesperetin Stimulates Cholecystokinin Secretion in Enteroendocrine STC-1 Cells

Kim, Hye Young; Park, Min; Kim, Kyong; Lee, Yu Mi; Rhyu, Mee-Ra

doi:10.4062/biomolther.2012.077

Cited by 46 publications

(27 citation statements)

References 16 publications

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“…HT and its glycoside HD (hesperetin 7‐rhamnoglucoside) are another two potent polyphenols. Kim et al () found that HT but not HD, induced gut hormone cholecystokinin secretion in STC‐1 cells through increasing intracellular Ca 2+ influx. The increases in intracellular Ca 2+ appears to be the primary trigger of GLP‐1 secretion (Tian & Jin, ), thus it is predictable that HT also stimulates GLP‐1 secretion.…”

Section: Discussionmentioning

confidence: 99%

Effect of food ingredients on glucagon‐like peptide‐1 secretion in STC‐1 and HuTu‐80 cells

Yue

Madsen

Hedemann

et al. 2019

Int J of Food Sci Tech

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Summary This study aims at identifying food ingredients that have potential to enhance satiety and therefore potentially can be used for preventing and treating obesity. To do so, effects of thirteen food ingredients on the secretion of gut satiety hormone glucagon‐like peptide‐1 (GLP‐1) in enteroendocrine STC‐1 and HuTu‐80 cells were investigated. First, the effects of food ingredients on cell viability were investigated. This was done to determine if the individual ingredient affected cell viability, and in case so, to determine the ingredient concentration below which, the cell viability was unaffected. Enzyme‐treated whey protein, palmitic acid, stearic acid, green tea extract, and hesperidin did not affect GLP‐1 secretion. Functional soy protein, fractionated functional soy protein, acetylated monoglyceride, N‐oleoylethanolamine, epigallocatechin‐3‐gallate, hesperetin, rosemary extract, and kale extract increased GLP‐1 secretion in at least one cell line. However, the effects of the eight potent ingredients on GLP‐1 secretion need to be further investigated in vivo.

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Section: Discussionmentioning

confidence: 99%

Effect of food ingredients on glucagon‐like peptide‐1 secretion in STC‐1 and HuTu‐80 cells

Yue

Madsen

Hedemann

et al. 2019

Int J of Food Sci Tech

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“…CCK release from STC-1 cells was determined based on previous reports 38 , 39 . Cells were grown overnight in 24-well plates (5 × 10 5 cells/well), washed and exposed to 0, 30, 100, or 300 μM MHBAs or the β-tricarbonyl model compound dissolved in a culture medium containing 0.3% DMSO for 60 min at 37 °C in 5% CO2/air humidity.…”

Section: Methodsmentioning

confidence: 99%

“…The cell line was purchased from ATCC (Manassas, VA, USA) and was maintained in DMEM containing 10% fetal bovine serum, 100 U/mL penicillin, and 100 μg/mL streptomycin (Gibco, Grand Island, NY, USA) at 37 °C in 5% CO 2 /air humidity. CCK release from STC-1 cells was determined based on previous reports 38,39 . Cells were grown overnight in 24-well plates (5 × 10 5 cells/well), washed and exposed to 0, 30, 100, or 300 μM MHBAs or the β-tricarbonyl model compound dissolved in a culture medium containing 0.3% DMSO for 60 min at 37 °C in 5% CO2/air humidity.…”

Section: Novel Object Recognition Test (Nort)mentioning

confidence: 99%

Hop bitter acids containing a β-carbonyl moiety prevent inflammation-induced cognitive decline via the vagus nerve and noradrenergic system

Ano

Ohya

Yamazaki

et al. 2020

Sci Rep

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The prevention of age-related cognitive decline and dementia is becoming a high priority because of the rapid growth of aging populations. We have previously shown that hop bitter acids such as iso-α-acids (IAAs) and matured hop bitter acids (MHBAs) activate the vagus nerve and improve memory impairment. Moreover, supplements with MHBAs were shown to improve memory retrieval in older adults. However, the underlying mechanisms have not been entirely elucidated. We aimed to investigate the effects of MHBAs and the common β-tricarbonyl moiety on memory impairment induced by the activation of microglia and the loss of the noradrenergic system. MHBAs and a model compound with β-tricarbonyl moiety were administered to LPS-inoculated mice and 5 × FAD Alzheimer’s disease (AD) model mice, following the evaluation in behavioral tests and microglial activation. To evaluate the association of noradrenaline with MHBAs effects, mice treated with N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP-4), a noradrenergic neurotoxin that selectively damages noradrenergic projections from the locus coeruleus, were subjected to the behavioral evaluation. MHBAs reduced brain inflammation and improved LPS-induced memory impairment. A model compound possessing the β-tricarbonyl moiety improved the LPS-induced memory impairment and neuronal loss via the vagus nerve. Additionally, the protective effects of MHBAs on memory impairment were attenuated by noradrenaline depletion using DSP-4. MHBAs suppressed the activation of microglia and improved the memory impairment in 5 × FAD mice, which was also attenuated by noradrenaline depletion. Treatment with MHBAs increased cholecystokinin production from the intestinal cells. Generally, cholecystokinin activates the vagal nerve, which stimulate the noradrenergic neuron in the locus ceruleus. Taken together, our results reveal that food ingredients such as hop bitter acids with a β-tricarbonyl moiety suppress microglial activation and improve memory impairment induced by inflammation or AD pathology via the activation of the gut-brain axis and noradrenergic system. Supplements with hop bitter acids, including MHBAs, might be a novel approach for the prevention of cognitive decline and dementia.

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“…AITC was used as a positive control. A TRP antagonist (RR, 100 μΜ) and a TRPA1 antagonist (HC-030031, 50 μΜ) were preincubated for 30 min before addition of the test agents [19].…”

Section: Determination Of Cck Releasementioning

confidence: 99%

“…The data are reported as the mean ± SEM of the ΔRFU. A TRP antagonist (RR, 100 μΜ) and a TRPA1 antagonist (HC-030031, 50 μΜ) were co-incubated with the calcium-indicator dye for 60 min [19].…”

Section: + ]I In Stc-1 Cellsmentioning

confidence: 99%

Naringenin stimulates cholecystokinin secretion in STC-1 cells

et al. 2014

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BACKGROUND/OBJECTIVES: Cholecystokinin (CCK), a hormone or neuropeptide, is secreted in response to intraluminal nutrients by enteroendocrine I-cells of the intestine and has important physiological actions related to appetite regulation and satiety. The stimulation on CCK secretion from the intestine is of potential relevance for body weight management. Naringenin (4',5,7-trihydroxyflavanone) and its glycoside naringin (naringenin 7-rhamnoglucoside) have been reported to have many biological functions. In the current study, we investigated the question of whether naringenin and naringin could stimulate CCK secretion and then examined the mechanisms involved in CCK release. MATERIALS/METHODS: STC-1 cells were used as a model of enteroendocrine cells. CCK release and changes in intracellular Ca 2+ ([Ca 2+ ]i) were measured after incubation of cells with naringenin and naringin for 1 h. RESULTS: Naringenin caused significant (P < 0.05) stimulation of CCK secretion, but naringin did not. In addition, regarding the secretory mechanisms, naringenin-induced CCK secretion involved increases in [Ca 2+ ]i, influx of extracellular Ca 2+ , at least in part, and activation of TRP channels, including TRPA1. CONCLUSION: Findings of this study suggest that naringenin could have a role in appetite regulation and satiety.

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Hesperetin Stimulates Cholecystokinin Secretion in Enteroendocrine STC-1 Cells

Cited by 46 publications

References 16 publications

Effect of food ingredients on glucagon‐like peptide‐1 secretion in STC‐1 and HuTu‐80 cells

Effect of food ingredients on glucagon‐like peptide‐1 secretion in STC‐1 and HuTu‐80 cells

Hop bitter acids containing a β-carbonyl moiety prevent inflammation-induced cognitive decline via the vagus nerve and noradrenergic system

Naringenin stimulates cholecystokinin secretion in STC-1 cells

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