• Title/Summary/Keyword: satiety response

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Chia seed (Salvia Hispanica L.) added yogurt reduces short-term food intake and increases satiety: randomised controlled trial

  • Ayaz, Aylin;Akyol, Asli;Inan-Eroglu, Elif;Cetin, Arzu Kabasakal;Samur, Gulhan;Akbiyik, Filiz
    • Nutrition Research and Practice
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    • v.11 no.5
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    • pp.412-418
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    • 2017
  • BACKGROUND/OBJECTIVE: Several studies have reported that consumption of Salvia Hispanica L.,commonly known as chia seed, may exert beneficial effects on health outcomes. The main purpose of this study was to examine the influence of chia seed consumption as a mid-morning snack on short-term satiety. SUBJECTS/METHODS: Subjects (n = 24) were tested using a randomized, cross-over design consisting of three mid-morning snacks. Yogurt with no chia seed, yogurt with 7 g chia seed, and yogurt with 14 g chia seed were given to subjects on different test days. After subjects were asked to report visual analog scale (VAS) scores on sensory outcomes, ad libitum lunch was served, and energy intake of individuals was measured. RESULTS: VAS scores indicated that participants reported significantly lower scores for hunger (P = 0.033), prospective food consumption (P = 0.031), amounts of food that could be consumed (P = 0.017), desire for sugary foods (P = 0.015), and higher scores for satiety (P = 0.031) on the test days with 7 g and 14 g chia seed. Energy intake of individuals during ad libitum lunch was significantly lower when they consumed yogurt with 7 g or 14 g chia seed (P = 0.037). CONCLUSIONS: The study demonstrated that chia seed consumption as a mid-morning snack may induce short-term satiety in healthy individuals.

Stomach clusterin as a gut-derived feeding regulator

  • Cherl NamKoong;Bohye Kim;Ji Hee Yu;Byung Soo Youn;Hanbin Kim;Evonne Kim;So Young Gil;Gil Myoung Kang;Chan Hee Lee;Young-Bum Kim;Kyeong-Han Park;Min-Seon Kim;Obin Kwon
    • BMB Reports
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    • v.57 no.3
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    • pp.149-154
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    • 2024
  • The stomach has emerged as a crucial endocrine organ in the regulation of feeding since the discovery of ghrelin. Gut-derived hormones, such as ghrelin and cholecystokinin, can act through the vagus nerve. We previously reported the satiety effect of hypothalamic clusterin, but the impact of peripheral clusterin remains unknown. In this study, we administered clusterin intraperitoneally to mice and observed its ability to suppress fasting-driven food intake. Interestingly, we found its synergism with cholecystokinin and antagonism with ghrelin. These effects were accompanied by increased c-fos immunoreactivity in nucleus tractus solitarius, area postrema, and hypothalamic paraventricular nucleus. Notably, truncal vagotomy abolished this response. The stomach expressed clusterin at high levels among the organs, and gastric clusterin was detected in specific enteroendocrine cells and the submucosal plexus. Gastric clusterin expression decreased after fasting but recovered after 2 hours of refeeding. Furthermore, we confirmed that stomachspecific overexpression of clusterin reduced food intake after overnight fasting. These results suggest that gastric clusterin may function as a gut-derived peptide involved in the regulation of feeding through the gut-brain axis.

Effect of plate size on meal energy intake in normal weight women

  • Ayaz, Aylin;Akyol, Asli;Cetin, Cansu;Besler, H. Tanju
    • Nutrition Research and Practice
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    • v.10 no.5
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    • pp.524-529
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    • 2016
  • BACKGROUND/OBJECTIVES: Use of smaller plates to control food intake is a commonly recommended strategy for restricting energy intake, despite conflicting results. Therefore, the aim of this study was to examine whether or not three different sizes of plates influence energy intake during a multi-itemed buffet meal in normal weight women. SUBJECTS/METHODS: This was a cross-over study conducted on 37 female participants aged 19-25 years with normal BMI levels. Participants were recruited from Hacettepe University and the surrounding community. On experimental days, participants ate a standard breakfast and were then randomly assigned to eat lunch using a small (19 cm), medium (23 cm), or large (28 cm) diameter plate. Visual analogue scale (VAS) scores on sensory and satiety outcomes were measured for all meals. Energy and macronutrient intakes during lunch were recorded. RESULTS: There was no evidence that use of a smaller plate size reduced energy or specific macronutrient intake during the free choice lunch meal. Multiple visits to the serving table were not associated with energy or macronutrient intake. Plate size did not affect VAS scores during the test days. CONCLUSIONS: Plate size did not influence energy intake, meal composition, or palatability in normal weight women during a multi-itemed open buffet lunch. Studies in natural settings at the population level are needed to clarify current outcomes.

Naringenin stimulates cholecystokinin secretion in STC-1 cells

  • Park, Min;Kim, Kyong;Lee, Yu Mi;Rhyu, Mee Ra;Kim, Hye Young
    • Nutrition Research and Practice
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    • v.8 no.2
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    • pp.146-150
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    • 2014
  • 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.

The Effect of Artificial Sweetener Use on Obesity (인공감미료 섭취가 비만에 미치는 영향)

  • Ju Sam Hwang
    • Archives of Obesity and Metabolism
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    • v.2 no.2
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    • pp.45-53
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    • 2023
  • Despite the emergence of obesity as a significant public health concern, artificial sweeteners have made their way into various food products due to the perception, that they serve as substitutes for sugar. Artificial sweeteners are used to supposedly achieve weight management and health improvement. However, their efficacy and safety remain debatable. Commonly used artificial sweeteners include aspartame, acesulfame potassium, saccharin, and sucralose. This article discusses the effects of artificial sweetener consumption on weight loss, appetite regulation, blood glucose control, and gut microbiota. Research findings, concerning the consumption of artificial sweeteners and their association with body weight, have shown inconsistencies between randomized controlled trials and cohort studies. Studies, comparing artificial sweeteners to sugar, have reported no significant differences in satiety. Although artificial sweeteners have no calories, they can affect blood sugar levels through the cephalic phase insulin response. A recent study suggested that artificial sweeteners influenced the occurrence of diabetes. Due to limitations in the study design, excluding diabetes-influencing factors was not feasible. The evidence showed that artificial sweeteners harbored potential health risks, necessitating further investigation. According to recent studies, the consumption of artificial sweeteners was associated with gut microbiota changes and individual blood sugar responses. It is important to note that artificial sweeteners cannot be considered safe alternatives to sugar, and further research is required.

Effect of JAK-STAT pathway in regulation of fatty liver hemorrhagic syndrome in chickens

  • Zhu, Yaling;Mao, Huirong;Peng, Gang;Zeng, Qingjie;Wei, Qing;Ruan, Jiming;Huang, Jianzhen
    • Animal Bioscience
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    • v.34 no.1
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    • pp.143-153
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    • 2021
  • Objective: To explore the molecular mechanisms of fatty liver hemorrhagic syndrome (FLHS) in laying hens, an experiment was conducted to reveal the differences in histopathological observation and gene expression between FLHS group and normal group. Methods: We compared the histopathological difference using hematoxylin and eosin staining and proceeded with RNA sequencing of adipose tissue to search differentially expressed genes and enriched biological processes and pathways. Then we validated the mRNA expression levels by real-time polymerase chain reaction and quantified protein levels in the circulation by enzyme-linked immunosorbent assay. Results: We identified 100 differentially expressed transcripts corresponding to 66 genes (DEGs) were identified between FLHS-affected group and normal group. Seven DEGs were significantly enriched in the immune response process and lipid metabolic process, including phospholipase A2 group V, WAP kunitz and netrin domain containing 2, delta 4-desaturase sphingolipid 2, perilipin 3, interleukin-6 (IL-6), ciliary neurotrophic factor (CNTF), and suppressor of cytokine signaling 3 (SOCS3). And these genes could be the targets of immune response and be involved in metabolic homeostasis during the process of FLHS in laying hens. Based on functional categories of the DEGs, we further proposed a model to explain the etiology and pathogenesis of FLHS. IL-6 and SOCS3 mediate inflammatory responses and the satiety hormone of leptin, induce dysfunction of Jak-STAT signaling pathway, leading to insulin resistance and lipid metabolic disorders. Conversely, CNTF may reduce tissue destruction during inflammatory attacks and confer protection from inflammation-induced insulin resistance in FLHS chickens. Conclusion: These findings highlight the therapeutic implications of targeting the JAK-STAT pathway. Inhibition of IL6 and SOCS3 and facilitation of CNTF could serve as a favorable strategy to enhance insulin action and improve glucose homoeostasis, which are of importance for treating obesity-related disorders for chickens.