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Cystic Fibrosis and Pancreatic Disease
Published in Praveen S. Goday, Cassandra L. S. Walia, Pediatric Nutrition for Dietitians, 2022
Elissa M. Downs, Jillian K. Mai, Sarah Jane Schwarzenberg
Malnutrition, as manifested by poor weight gain and slowing of linear growth, is common in people with CF who may not have the benefit of CFTR modulator therapy and/or have advanced disease. This is multifactorial, with contributions from hypermetabolism (chronic inflammation or infections, increased work of breathing and coughing, pulmonary exacerbations), malabsorption, problematic mealtime behaviors (picky eating, food refusal, grazing), or disordered eating behaviors. To prevent malnutrition and improve outcomes, a high-energy, high-fat diet is recommended, when indicated.
Oxidative Stress and Inflammation
Published in Abhai Kumar, Debasis Bagchi, Antioxidants and Functional Foods for Neurodegenerative Disorders, 2021
Varsha Rana, Dey Parama, Sosmitha Girisa, Choudhary Harsha, Ajaikumar B. Kunnumakkara
Tobacco or cigarette smoking has often been linked to reduced antioxidant levels and is known to obstruct the DNA repair mechanism. It results in an increased level of 8-OHdG, a marker of DNA damage, in patients with lung cancer (Cao et al., 2016). Oxidative DNA damage caused by smoking correlates with various diseases such as Alzheimer’s, chronic obstructive pulmonary disease (COPD), and lung cancer (Durazzo et al., 2014; Zuo et al., 2014; Cao et al., 2016). Khan et al. (2006) reported that obesity increases systemic oxidative stress independently. Furthermore, a clinical study conducted by Keaney and colleagues also established the association of obesity as an independent risk factor for oxidative stress (Keaney et al., 2003). Improper diet can also be considered a vital risk factor for oxidative stress. For instance, an in-vivo study demonstrated that a high fat diet (HFD) induced dramatic neuronal damage in the hippocampus of the brain (Ledreux et al., 2016). Another in-vivo study revealed that HFD along with exposure to real-world ambient particulate matter (PM) dramatically and synergistically increased inflammation as well as oxidative stress in the liver (Ding et al., 2019). High sucrose diet (HSD) or hyperglycemia was also reported to induce oxidative stress and further aggravate diabetic complications (King and Loeken, 2004). Consistent with these findings, HSD in combination with HFD was also found to exhibit increased oxidative stress and inflammation in male Sprague-Dawley rats (Sweazea et al., 2010).
Insulin Resistance and Glucose Regulation
Published in Awanish Kumar, Ashwini Kumar, Diabetes, 2020
A common perception and fact is that the regular consumption of a high-fat diet results in diet-induced obesity. High fat intake is also said to be a cause of T2DM, independent of obesity. This risk is subjected to the type of fatty acids consumed in the diet. The fatty acid composition of skeletal muscle cells varies with the change in dietary fatty acids. It was shown long ago that T2DM patients had a greater amount of saturated fatty acids in their plasma as compared to non-diabetic subjects, who had more linoleic acid. The insulin sensitivity of skeletal muscle cells was directly proportional to the amount of long-chain polyunsaturated fatty acids in the cell membrane [36]. The replacement of safflower oil with fish oil (rich in omega-3 fatty acids) in a rat diet prevented the development of insulin resistance in hepatocytes and skeletal muscle cells. Diets rich in saturated fats result in elevated TG in hepatocytes. In a breakthrough study, it was found that skeletal muscle insulin resistance was directly related to the amount of triglyceride accumulation in those cells, while the percentage of long chain omega-3 fatty acids was directly related to the insulin stimulated glucose uptake; omega-6 fatty acid rich diets were also involved in stimulating insulin resistance [49].
Effects of saturated versus unsaturated fatty acids on metabolism, gliosis, and hypothalamic leptin sensitivity in male mice
Published in Nutritional Neuroscience, 2023
Jesús Fernández-Felipe, Maria Valencia-Avezuela, Beatriz Merino, Beatriz Somoza, Victoria Cano, Ana B. Sanz-Martos, Laura M. Frago, Maria S. Fernández-Alfonso, Mariano Ruiz-Gayo, Julie A. Chowen
There is a clear difference in the response to the two fatty acid enriched diets used in these studies and this is most likely due to their different fatty acid compositions as other components were very similar. However, identification of the nutrients responsible for the different metabolic response to these diets compared to that observed in chow fed mice is less direct. Not only is the fatty acid content different, but also that of proteins and carbohydrates, as well as of fiber and some vitamins and minerals, all of which could affect metabolism. Thus, one can only conclude that these diets enriched in fatty acids induce weight gain and other metabolic changes compared to a standard chow diet, which is assumed to be a healthy diet for these animals. Indeed, the response to high fat diet intake depends on the control diet used for comparison [55].
Role of the microbiota in circadian rhythms of the host
Published in Chronobiology International, 2020
A high-fat diet alters the alpha- and beta-diversity of the microbial community and reduces the number of OTUs exhibiting significant oscillation patterns (Leone et al. 2015). It is observed that a high-fat diet leads to increases in Firmicutes and decreases in Bacteroidetes compared to controls on regular chow. (Murakami et al. 2016) A high-fat diet induces Bmal1, Clock, Per2, and Cry1 expression in the mediobasal hypothalamus, but suppresses their expression in the liver of mice (Leone et al. 2015). The induced remodeling of the gut microbiota causes the induction and activation of the transcription factor PPARγ, which in turn reprograms the hepatic circadian clock (Murakami et al. 2016). A hypocaloric diet speeds up the re-entrainment to a shifted light/dark cycle, while a high-fat diet slows it down. This also indicates that the number of calories may be of higher importance than the actual metabolites of a high-fat diet (Oosterman et al. 2015).
Uridine dynamic administration affects circadian variations in lipid metabolisms in the liver of high-fat-diet-fed mice
Published in Chronobiology International, 2019
Yilin Liu, Yumei Zhang, Jie Yin, Zheng Ruan, Xin Wu, Yulong Yin
Circadian rhythmicity is the ability of most organisms to adapt to the environment and play a major role in orchestrating daily physiology. The circadian system is a complex feedback network that is closely connected to metabolic homeostasis and involves interactions between the central nervous system and peripheral tissues (Green et al. 2008). Desynchronization between the central and peripheral clocks, by altering the timing of food intake and diet composition can lead to uncoupling of peripheral clocks from the central pacemaker, and to the development of metabolic disorders (Oosterman et al. 2015). High-fat diet, one of the unhealthy lifestyle choices, is part of the cause of increased obesity. It has been reported HFD causes the reprogramming of the clock and clock-controlled genes, resulting in a reorganization of the coordinated oscillations between coherent transcripts and metabolites (Eckel-Mahan et al. 2013; Kohsaka et al. 2007). For example, the circadian rhythm of insulin secretion, glucocorticoid regulation, and adiponectin signaling pathway were disrupted by the HFD intake (Appiakannan et al. 2019; Barnea et al. 2010; Honma et al. 2016).