Overweight and obesity are one of the major health problems of modern civilization as they carry a high risk to develop chronic diseases such as metabolic syndrome, type II diabetes (T2D), and non–alcoholic fatty liver disease. T2D, affecting more than 450 million patients worldwide, does not only lead to hyperglycemia but is highly associated with micro- and macrovascular disease such as chronic kidney disease, neuropathy or cardiovascular disease, and is even associated with increased mortality.
Chronic inflammation in adipose tissue has been described as a mechanism for obesity-related complications
Adipose tissue is not a passive reservoir for energy but a complex endocrine, paracrine and autocrine organ which orchestrates a vast number of cytokines referred to as adipokines.
Brown and beige adipocytes which are located within white adipose tissue are responsible for the generation of non–shivering thermogenesis and thus protect against metabolic disorders. Obesity and insulin resistance are characterized by impaired beige adipogenesis and an altered brown-versus-white plasticity and a hypertrophic adipocyte phenotype. Low-grade chronic inflammation in adipose tissue has been described as a mechanism for obesity-related complications. While predominately anti–inflammatory cytokines are secreted from adipose tissue of healthy, lean subjects, higher amounts of proinflammatory adipokines are typically seen in obese individuals.
In states of overnutrition adipose tissue expansion leads to adipocyte hypertrophy which is often associated with hypoxia and increased expression of Hif1α. The latter is associated with decreased β-oxidation, dysregulation of adipokines, and induction of necrosis.
Switching diet from a harmful to a more beneficial one is sufficient to reverse adipose tissue inflammation
Excessive weight loss by reduced caloric intake has extensively been demonstrated to improve glucose metabolism and reverse adipocyte dysfunction. Adipocyte dysfunction is a hallmark of obesity related diseases such as insulin resistance and non–alcoholic fatty liver disease (NAFLD). While the concept of metabolically healthy obesity underlines its pivotal role in obesity related disorders, therapies that specifically address adipocyte dysfunction are very limited. Pronounced weight loss resulting has extensively shown to improve systemic glucose metabolism and adipocyte function , however, it is frequently associated with significant risk of long-term complications such as malabsorption or bone disease. Weight loss by caloric restriction has also been shown to improve whole body energy metabolism and adipose tissue function, however, maintenance of weight loss is commonly very challenging and often frustrating.
Switching the diet is sufficient to reverse Western diet induced alterations in adipogenesis and adipose tissue inflammation.
Western-type diets, which are characterized by increased intake of high glycemic index refined foods rich in sugar, salt, saturated fat, trans fat and oxidized fat, processed foods, and red meat.
The researchers suggest that switching the diet from a harmful Western diet to a Healthy diet is sufficient to improve adipose tissue inflammation. Switching diet from a Western diet to a healthy diet reduces adipocyte size and Hif1α expression in white and brown adipose tissue.
Dietary intake of saturated fatty acids and sucrose is accompanied by a shift toward larger adipocytes with diminished insulin sensitivity. In contrast, feeding a Western diet induces whitening of brown adipose tissue and inhibits beiging of white adipose tissue in the long-term.
Reference
-Folie S, et al. Changing the dietary composition improves inflammation but not adipocyte thermogenesis in diet-induced obese mice. The Journal of Nutritional Biochemistry.2022.
