Cafeteria Diet Is a Robust Model of Human Metabolic Syndrome With Liver and Adipose Inflammation: Comparison to High‐Fat Diet

Abstract

Obesity has reached epidemic proportions worldwide and reports estimate that American children consume up to 25% of calories from snacks. Several animal models of obesity exist, but studies are lacking that compare high-fat diets (HFD) traditionally used in rodent models of diet-induced obesity (DIO) to diets consisting of food regularly consumed by humans, including high-salt, high-fat, low-fiber, energy dense foods such as cookies, chips, and processed meats. To investigate the obesogenic and inflammatory consequences of a cafeteria diet (CAF) compared to a lard-based 45% HFD in rodent models, male Wistar rats were fed HFD, CAF or chow control diets for 15 weeks. Body weight increased dramatically and remained significantly elevated in CAF-fed rats compared to all other diets. Glucose- and insulin-tolerance tests revealed that hyperinsulinemia, hyperglycemia, and glucose intolerance were exaggerated in the CAF-fed rats compared to controls and HFD-fed rats. It is well-established that macrophages infiltrate metabolic tissues at the onset of weight gain and directly contribute to inflammation, insulin resistance, and obesity. Although both high fat diets resulted in increased adiposity and hepatosteatosis, CAF-fed rats displayed remarkable inflammation in white fat, brown fat and liver compared to HFD and controls. In sum, the CAF provided a robust model of human metabolic syndrome compared to traditional lard-based HFD, creating a phenotype of exaggerated obesity with glucose intolerance and inflammation. This model provides a unique platform to study the biochemical, genomic and physiological mechanisms of obesity and obesity-related disease states that are pandemic in western civilization today.

Exposure of neonatal rats to maternal cafeteria feeding during suckling alters hepatic gene expression and DNA methylation in the insulin signalling pathway

“…The combination of high fat with high sodium, sugars, saturated fat and cholesterol and low in fibre and micronutrients makes the protocol more closely aligned with dietary patterns observed in the humans than conventional purified high-fat diets used in rodent studies (Crozier et al 2006;Kant 2004). It is considered the most effective tool for modelling the effects of ''non-prudent'' dietary patterns and dietinduced obesity in humans (Sampey et al 2011). The study examined two key hypotheses, and the data generated support the assertion that maternal cafeteria feeding during lactation programmes metabolic function through long-term alteration of expression of the insulin signalling and other metabolic pathways.…”

Effects of liraglutide and sibutramine on food intake, palatability, body weight and glucose tolerance in the gubra DIO-rats

“…Since then, numerous DIO models have been published using the general approach whereby diets composed of alternating components of fat and carbohydrates are administered to normal, lean rats or mice over long periods [8,10,20] . The so-called cafeteria diets, where animals have a choice of various palatable foods such as chocolate, peanuts etc, encourages overeating and hence provides highly relevant models for examining human diets in rodents [15,[21][22][23] .…”

Leptin signal transduction underlies the differential metabolic response of LEW and WKY rats to cafeteria diet

“…Furthermore, although the interactions between genes and the environment that are associated with the development of obesity are not fully understood, studies of inbred animal strains showed susceptibility to diet-induced obesity, whereas other strains show resistance, therefore suggesting that the genetic background contribute to the variability in obesogenic phenotypes between individuals (Hu et al 2004, Koza et al 2006, Parks et al 2013. Diet-induced obesity models, such as the cafeteria (CAF) diet-induced obesity, are considered to be a robust model of the human metabolic syndrome and its related pathologies (Sampey et al 2011). In a CAF diet, obesity is induced as consequence of hyperphagia resulting from the voluntary intake of highly palatable and energy-dense cafeteria-style foods present in Western-type diets instead of the standard chow (Sampey et al 2011).…”

“…Diet-induced obesity models, such as the cafeteria (CAF) diet-induced obesity, are considered to be a robust model of the human metabolic syndrome and its related pathologies (Sampey et al 2011). In a CAF diet, obesity is induced as consequence of hyperphagia resulting from the voluntary intake of highly palatable and energy-dense cafeteria-style foods present in Western-type diets instead of the standard chow (Sampey et al 2011).…”