Abstract
Type 2 Diabetes mellitus (T2DM) is an evident growing disease that affects different cultures throughout the world. T2DM occurs under the influence of three main factors: the genetic background, environmental and behavioral components. Obesity is strongly associated to the development of T2DM in the occident, while in the orient most of the diabetic patients are considered lean. Genetics may be a key factor in the development of T2DM in societies where obesity is not a recurrent public health problem. Herein, two different models of rats were used to understand their differences and reliability as experimental models to study the pathophysiology of T2DM, in two different approaches: the genetic (GK rats) and the environmental (HFD-induced obese rats) influences. GK rats were resistant to weight gain even though food/energy consumption (relative to body weight) was higher in this group. HFD, on the other hand, induced obesity in Wistar rats. White adipose tissue (WAT) expansion in this group was accompanied by immune cells infiltration, inflammation and insulin resistance. GK rats also presented WAT inflammation and insulin resistance; however, no immune cells infiltration was observed in the WAT of this group. Liver of HFD group presented fat accumulation without differences in inflammatory cytokines content, while liver of GK rats didn’t present fat accumulation, but showed an increase of IL-6 and IL-10 content and glycogen. Also, GK rats showed increased plasma GOT and GPT. Soleus muscle of HFD presented normal insulin signaling, contrary to GK rats, which presented higher content of basal phosphorylation of GSK-3β. Our results demonstrated that HFD developed a mild insulin resistance in Wistar rats, but was not sufficient to develop T2DM. In contrast, GK rats presented all the typical hallmarks of T2DM, such as insulin resistance, defective insulin production, fasting hyperglycemia/hyperinsulinemia and lipid plasma alteration. Thus, on the given time point of this study, we may conclude that only GK rats shown to be a reliable model to study T2DM.
Highlights
By 2030, diabetes mellitus (DM) will be the 7th leading cause of death worldwide, staying behind only of ischemic heart diseases, cerebral disease, HIV/AIDS, Chronic Obstructive Pulmonary Disease (COPD), lower respiratory infections, and trachea, bronchus and lung cancer [1]
Goto Kakizaki (GK) rats were resistant to weight gain, showing, after 8 week treatment, 28% and 42% less gain when compared to the control group and High-fat diet (HFD) fed animals, respectively (Fig 1A and 1B)
When energy consumption was measured, GK rats consumed more energy per day per Kg than the control and HFD groups, when food and energy intake were normalized by the body weight (Fig 1F)
Summary
By 2030, diabetes mellitus (DM) will be the 7th leading cause of death worldwide, staying behind only of ischemic heart diseases, cerebral disease, HIV/AIDS, Chronic Obstructive Pulmonary Disease (COPD), lower respiratory infections, and trachea, bronchus and lung cancer [1]. The incidence of DM has risen vertiginously and, in 2014, as claimed by the World Health Organization (WHO), reached the hallmark of 422 million individuals [2]. This augmentation is mainly because of unhealthy dietary habits, like increased intake of sugar, fats, processed foods, and sweetened beverages, related to low consumption of fruits and vegetables, as well as sedentary lifestyle. Development of T2DM is due to a combination of three different factors: genetic, environmental and behavioral [8]. We aim to compare two of the components that interfere in T2DM development: genetic versus environmental (diet) factors
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