Obesity Is a Major Health Problem: Causes and Natural History
Susan L. McElroy, David B. Allison, George A. Bray in Obesity and Mental Disorders, 2006
Epidemiologic data suggest that a high-fat diet is associated with obesity. The relative weight in several populations, for example, is directly related to the percentage of dietary fat in the diet (36–38). A high-fat diet introduces palatable foods into the diet, with a corresponding increase in energy density (i.e., lesser weight of food for the same number of calories). This makes over-consumption more likely. Differences in the storage capacity for various macronutrients also may be involved. The capacity to store glucose as glycogen in liver and muscle is limited and needs to be replenished frequently. This contrasts with fat stores, which are more than 100 times the daily intake of fat. This difference in storage capacity makes eating carbohydrates a more important physiologic need that may lead to overeating when dietary carbohydrate is limited and carbohydrate oxidation cannot be reduced sufficiently.
Insulin Resistance and Glucose Regulation
Awanish Kumar, Ashwini Kumar in 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].
Towards a New Theory of Antioncogenesis
Nate F. Cardarelli in Tin as a Vital Nutrient:, 2019
Low blood cholesterol also plays a role in carcinogenesis. Williams et al. note that lethal carcinoma of the colon is three times as likely in men with low cholesterol (below 190 mg/ℓ), although this did not appear to be true in women.22 In another study low blood cholesterol (below 180 mg/ℓ) was noted in Hawaiian males of Japanese descent dying from stomach, liver, and lung cancer.23 In a Puerto Rico study excess deaths from stomach and esophageal cancer in men 45 to 55 years of age correlated with low cholesterol levels.24 Morrison and Glueck have aptly summarized the above and other findings by noting that low blood cholesterol in combination with a high fat diet leads to greater incidence of cancer, and high blood cholesterol with a high fat diet increases the incidence of coronary heart disease.25 Kark et al. reported on an inverse relationship between malignant neoplasia and serum cholesterol.26
The metabolic and neuroinflammatory changes induced by consuming a cafeteria diet are age-dependent
Published in Nutritional Neuroscience, 2019
Deborah Teixeira, Ana Lucia Cecconello, Wania Aparecida Partata, Luciano Stürmer de Fraga, Maria Flávia Marques Ribeiro, Renata Padilha Guedes
Multiple studies have demonstrated the effect of high-fat diet on brain function in animal models and in humans.3,11,12 Various experimental models to induce obesity have been described, including transgenic animals, high-fat defined diets, and the cafeteria diet.13–15 Here, we used the cafeteria diet because of its low cost and similarity to a typical Western diet. In this model, animals are fed with regular chow and also have free access to highly palatable foods rich in simple sugars and saturated fat. Thus, the cafeteria diet mimics unhealthy foods regularly consumed by humans. Also, it has been shown that the cafeteria diet is a more representative model of human obesity than defined high-fat diets, thus making it well suited to investigations into the physiological mechanisms of obesity.16
Characterization of free fatty acid receptors expression in an obesity rat model with high sucrose diet
Published in Journal of Receptors and Signal Transduction, 2018
Fabián Meza-Cuenca, J. M. L. Medina-Contreras, Patrick Mailloux-Salinas, Luis A. Bautista-Hernández, Beatríz Buentello-Volante, Alfredo Domínguez-López, Yonathan Garfias, P. Valentín Correa-López, Víctor M. Bautista de Lucio, Guadalupe Bravo
Twenty weeks of high sucrose diet in rats produced an increased weight (obesity), an elevation of total cholesterol and triglycerides plasma levels with statistical differences without achieved diabetes (plasmatic glucose levels) compared with the normal diet group (control), which is consistent with previous standardizations in our laboratory [9]. There is evidence that consumption of high-fat diet increases total energy intake and that excess dietary fat is stored with a greater efficiency than similar excess of dietary carbohydrate and protein. In preclinical trials, the rats gained weight rapidly and could became quite obese on this rate, and they tend to select and consume a high proportion of energy from fat. However, it has been suggested that animals actually become more obese with cafeteria diets than with high-fat diets, indicating perhaps, a greater hyperphagia arising from the food variety [10]. The effects of added sugars on various chronic conditions are highly controversial [11]. On the other hand, there are studies that have been showed that liquid diets promoted greater body weight gain when fed over long periods, compared with powdered or pelleted dry diets [10].
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).
Related Knowledge Centers
- Fatty Acid
- Glucose
- Ketone Bodies
- Protein
- Liver
- Brain
- Epilepsy
- Carbohydrate
- Low-Carbohydrate Diet
- Triglyceride