Shifts in Diet from High Fat to High Carbohydrate Improved Levels of Adipokines and Pro-inflammatory Cytokines in Mice Fed a High-fat Diet

Abstract

Abstract. High-fat diets induce an expansion of the adipose tissue (aT) that can be characterized by chronic low-grade inflammation. AT is an important source of adipokines and pro-inflammatory cytokines. The purpose of this study was to evaluate the effects of a shift from a high-fat diet to high-carbohydrate (CHO) diet on the blood levels of adipokines and pro-inflammation cytokines in mice fed a high-fat diet. Six-week-old male C57BL/6 mice were fed a high-fat diet (40% of the total calories) for 9 weeks to induce obesity, and then the diet was shifted to a high CHO diet (70% of the total calories) for 3 weeks. Body weight and organ weight as well as blood lipid levels were measured. The serum levels of adipokines and pro-inflammatory cytokines were analyzed. Shifting the diet from high fat to high CHO decreased significantly body weight, adipose tissues, and liver weight (p < 0.05). The lipid blood levels (TG, Total-chol, and LDLchol) decreased. The leptin and resistin blood levels significantly decreased after the diet was shifted to a high-CHO diet (p < 0.05); however, the adiponectin concentrations did not change. The IL-6 levels were also significantly decreased by the high-CHo diet (p < 0.05). The IL-13 serum levels were significantly increased by the high-CHO diet (p < 0.05). Further, the serum levels of the TNF-α and supernatant IL-1β concentrations in mice fed a high-carbohydrate diet were significantly increased after the mice were shifted to a high-fat diet. On the other hand, the serum IL-4 and supernatant levels did not change. Conclusively, reduction of body weight and adipose tissues through shifts from a high-fat diet to a high-carbohydrate diet effectively improved low-grade inflammation states in mice fed a high-fat diet. Particularly, the reduction of body weight was associated with the levels of leptin, resistin, and IL-6.

Effect of Citrus Flavonoids, Naringin and Naringenin, on Metabolic Syndrome and Their Mechanisms of Action

“…On the other hand, inflammatory cytokines such as TNF-a and IL-6 may also cause dysfunction of peripheral insulin receptor and insulin resistance and ultimately increase glucose concentrations in plasma (88,89). A high-fat diet increased inflammatory cytokines and caused insulin resistance and hyperglycemia (90,91). The hypoglycemic effect of naringin is well documented ( Table 4) (80,92).…”

Differential Proinflammatory and Oxidative Stress Response and Vulnerability to Metabolic Syndrome in Habitual High-Fat Young Male Consumers Putatively Predisposed by Their Genetic Background

“…Indeed, a study carried out in mice revealed that the inflammatory state associated with obesity appears to be partly triggered by high fat diet and excessive weight [22]. Furthermore, the composition and quantity of the fat content of a meal seems to be directly related to the magnitude of the postprandial inflammatory response [23].…”

Novel mechanisms of Na+ retention in obesity: phosphorylation of NKCC2 and regulation of SPAK/OSR1 by AMPK

“…C57BL/6 mice fed a HFD develop progressive insulin resistance and provide a good model for studying obesity-related hyperinsulinemia (55). After mice receive a HFD for 3 mo, there is an approximately twofold increase in plasma insulin, which is much more akin to the changes found in human obesity than those seen in ZO rats (24,55). Administration of a HFD also produces hyperlipidemia, hyperleptinemia, and hypoadiponectinemia in C57BL/6 mice, thereby mimicking the changes seen with metabolic syndrome in humans (24).…”