Perrard mice al. Fat exact combinations are not time leading to differences in nutrient levels from batch to batch 12, Clin Inflammation. Proposed conceptual link between high-fat diet feeding and renal amyloidosis. The nutrient levels are naturally subject of change and therefore their exact content is hard to define The increased presence of adipocytes largely changes the hematopoietic stem cell niche in the Diet increade increase sets up a niche for tumor cells, increasing their proliferation by IL-6 and Janus Kinase 2 JAK2. Asha, High.
In recent years, chronic overnutrition, such as consumption of a high-fat diet HFD, has been increasingly viewed as a significant modifiable risk factor for diseases such as diabetes and certain types of cancer. However, the mechanisms by which HFDs exert adverse effects on human health remains poorly understood. Here, this paper will review the recent scientific literature about HFD-induced inflammation and subsequent development of diseases and cancer, with an emphasis on mechanisms involved. Given the expanding global epidemic of excessive HFD intake, understanding the impacts of a HFD on these medical conditions, gaining great insights into possible underlying mechanisms, and developing effective therapeutic strategies are of great importance. At present, obesity has reached epidemic proportions. It develops from an imbalance of energy homeostasis and contributes dramatically to the global disease burden, predisposing individuals to chronic diseases such as type 2 diabetes mellitus T2DM, cardiovascular disease CVD, and certain types of cancer 1, 2. Excessive consumption of high fat diets HFDs has undoubtedly exacerbated the obesity epidemic and the development of obesity-related metabolic disorders 3, 4. Despite substantial work demonstrating that obesity develops from an imbalance between energy intake and energy expenditure, the underlying mechanisms for the detrimental effects of HFDs seem to be more complicated than the simple concept of energy imbalance 5. In this context, a better understanding of the pathogenesis of HFD-driven metabolic disorders may help to reduce the disease burden worldwide. This review will elaborate on the precise pathology and etiology of diseases induced by a HFD, and will evaluate the possibility of therapeutic targeting of free fatty acids FFAs and low-grade systemic inflammation to reduce HFDs-stimulated diseases. Following the ingestion of HFDs, inflammation develops in the central nervous system CNS including the hypothalamus and in the peripheral tissues including the liver, adipose tissue, skeletal muscle, and intestine 6. Concerning the development of chronic systemic inflammation, alterations in the gut microbiota triggered by HFDs and direct effects of FFAs on intestinal cells may be the first step 7.
Iglewski et al. Suehiro, T. Macrophage PPAR gamma is required for normal skeletal muscle and hepatic insulin sensitivity and full antidiabetic effects of thiazolidinediones. Middelbeek, K. Extensive recent publications describe decreased autophagy [ 89, 90 ] and in particular mitophagy [ 91 ] as pathogenic in T2DM and HFD mouse models. High fat diet increases melanoma cell growth in the bone marrow by inducing osteopontin and interleukin 6. A2A adenosine receptors control pancreatic dysfunction in high-fat-diet-induced obesity. Pathophysiology of human visceral obesity: an update. In contrast, other human and animal studies have shown that HFDs induced higher BMD because of elevated mechanical loading 73, Therefore, the cafeteria diet CAF model was introduced. Acknowledgments We acknowledge Davith de Vries for his work on the amyloid phenotype, Danny Kor, Marjo van de Waarenburg, Henk Moorlag and Karin Toet for their laboratory assistance, Inge Vreeswijk Baudoin for her help on hemodynamic measurements, and Peter Zwiers and Arjen Petersen for their technical assistance on the animal experiments.
Thank you for visiting nature. To obtain the best experience, we recommend you use a more up to date browser or turn off compatibility mode in Internet Explorer. The aim of the present study was to compare different diets used to induce obesity in a head-to-head manner with a focus on insulin resistance and vascular dysfunction. In conclusions, CAF and HFD are both reliable mouse diets in inducing visceral obesity, glucose intolerance and insulin resistance.