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Gene Therapy and Gene Correction
Published in Yashwant V. Pathak, Gene Delivery Systems, 2022
Manish P. Patel, Sagar A. Popat, Jayvadan K. Patel
Hunger regulations: Neuropeptide (NPY), agouti-related peptide (AgRP) and GABA are three neurotransmitters that works in the hypothalamus to stimulate appetite (orexigenic). By decreasing this neurotransmitter, we can suppress hunger, which leads to less food intake and causes less chance of deposition of adipose tissue in large amounts. Leptin is a hormone which keeps a check on hunger. It is secreted from adipose tissue, which inhibits the secretion of neuropeptide Y and also causes activation of pro-opiomelanocortin (POMC) neurons (Kalra et al. 2005; Boghossian et al. 2005). POMC is part of the melanocortin system and produces α-MSH, which has a very important role in appetite suppression.
Epigenotoxicity: a danger to the future life
Published in Journal of Environmental Science and Health, Part A, 2023
Farzaneh Kefayati, Atoosa Karimi Babaahmadi, Taraneh Mousavi, Mahshid Hodjat, Mohammad Abdollahi
Another study showed a relation between altered histone acetylation and its effect on acetyl-CoA and metabolic pathways; thereby, obesity linkage with epigenetic histone modifications was proved.[130] A recent case-control study also reported four miRNAs’ roles in epigenetic regulation, including miR-328-3p, miR-1301-3p, miR-4685-3p, and miR-6803-3p of childhood obesity which correlates with the etiology of other diseases such as cancer or CVDs.[131] In another study, transgenerational obesity in a one-year-old F3 generation of rats was observed as the result of exposure to a hydrocarbon mixture involving jet fuel (JP-8) and through changes in DNA methylation patterns.[200] Since obesity is a complex disease with different mechanisms, epigenetic changes can affect different pathways. Hypermethylation of the proopiomelanocortin promoter gene inhibits satiety; thus, it correlates with gain weight and obesity. Leptin is a signal for energy homeostasis. Leptin dysfunction in adipose tissue due to hypomethylation of its gene and miR-200a, miR-200b, and miR-429 upregulation, also has a key role in obesity.[201]
Evaluation of sucrose-enriched diet consumption in the development of risk factors associated to type 2 diabetes, atherosclerosis and non-alcoholic fatty liver disease in a murine model
Published in International Journal of Environmental Health Research, 2021
Carolina Gabriela Plazas Guerrero, Selene De Jesús Acosta Cota, Francisco Humberto Castro Sánchez, Marcela De Jesús Vergara Jiménez, Efrén Rafael Ríos Burgueño, Juan Ignacio Sarmiento Sánchez, Lorenzo Antonio Picos Corrales, Ulises Osuna Martínez
Otherwise, high-sucrose consumption promotes higher insulinemic responses which triggers signals that are important in the control of food intake (Petykó et al. 2009). Insulin has an anorexigenic effect by decreasing the expression of orexigenic peptide Neuropeptide Y (NPY) and stimulating other satiety signals such as CCK and corticotropin-releasing hormone (CRH) (Hita et al. 2006). Insulin also stimulates leptin synthesis by adipocytes which increases satiety and decreases food intake since leptin acts on the hypothalamus by inhibiting the synthesis of NPY and increases the expression of anorexigenic peptides such as CRH (Sánchez 2005; Hita et al. 2006). This possible increase in blood leptin levels has already been observed in previous studies with mice fed with a high-sucrose diet (Oliveira et al. 2014; Castellanos Jankiewicz et al. 2015; Harris 2018).
Dietary Intake and Appetite Hormone Patterns among Mothers Participating in the Supplemental Nutrition Assistance Program: A Pilot Study
Published in Journal of Hunger & Environmental Nutrition, 2021
Megan M. Oberle, Eliza Whiteman Kinsey, Terri H. Lipman, Carolyn Cannuscio, Amy Hillier, Virginia A. Stallings
Calorie restriction has been associated with alterations in feeding behaviors, appetite-stimulating and appetite-suppressing hormones, and weight regulation in both animal models and human studies.27–31 An example of voluntary calorie restriction is the Muslim month of fasting, Ramadan, in which observers do not eat between dawn and sunset for one month. Calorie restriction during Ramadan was associated with increased appetite stimulation (ghrelin and neuropeptide Y concentrations), decreased appetite suppression (leptin concentrations), and increased intake of fat.32–35 Calorie restriction has been associated with a state of relative leptin deficiency, which can result in decreased energy expenditure, decreased appetite suppression, and lead to excess calorie consumption when food becomes available.35–37 Although short-term weight loss has been reported with intermittent calorie restriction, Ramadan observers regained weight once typical eating patterns were resumed.38–43 Decreases in appetite suppression and increases in appetite-stimulating hormone concentrations are protective neuroendocrine responses to caloric restriction and weight loss. SNAP participants may exhibit these same protective neuroendocrine responses when they experience calorie restriction, leading to excess calorie consumption when SNAP benefits are renewed, thus perpetuating the SNAP cycle and contributing the increased risk of BMI elevation in SNAP participants.