High-fat feeding and staphylococcus intermedius infection impair beta cell function and insulin sensitivity in mongrel dogs

Abstract

As obesity is a state of low-grade inflammation, we aimed to investigate the combined effect of high-fat diet and bacterial infection on beta-cell function and insulin sensitivity in dogs. We used 20 healthy, male, mongrel dogs randomly divided into four groups: control group-healthy, non-obese dogs; infected group-non-obese dogs with experimentally induced infection (Staphylococcus intermedius); obese group-obese dogs (after 90 day high-fat diet) and obese-infected group-obese dogs with experimentally induced infection (Staphylococcus intermedius). To evaluate insulin sensitivity and beta-cell function an intravenous glucose tolerance test (IVGTT) was performed. Plasma insulin increased in all group after glucose infusion. The lowest values were found in obese-infected group. Blood glucose also increased on 3 min after glucose infusion and then gradually decreased. In obese-infected group glucose concentration on 30 min was still significantly higher than initial levels, while in other groups glucose concentration returned to the initial values. The lowest rate of glucose elimination was found in infected group. In dogs of obese group and obese-infected group AUC(ins 0-60 min) was lower compared to controls. AUC(glucose 0-60 min) values were lowest in infected group, while in obese-infected group values were the highest. Levels of I/G in dogs of obese-infected group were significantly lower compared to controls and infected group. In conclusion, these results reveal that infection in obese dogs leads to impaired glucose tolerance, which is result of impairment in both insulin secretion and insulin sensitivity.

Effects of bacterial infection on insulin secretory capacity of human adult pancreatic islets

“…5 One study on dogs has demonstrated that the lowest rate of glucose elimination was in a group infected with Staphylococcus intermedius. 8 Infection causes marked changes in whole body glucose metabolism as a result of acceleration in endogenous glucose production, due to increased gluconeogenesis. 9 It has been shown that acute infection in humans causes insulin resistance and glucose intolerance.…”

Role of cytosolic and calcium independent phospholipases A2 in insulin secretion impairment of INS‐1E cells infected by S. aureus

“…Bacterial infection can lead to the impairment in insulin secretion [21] but the system(s) responsible of this effect has not been established. Attractive candidates are the PLA 2 s because their activity during insulin release by b cells.…”

“…Participation of PLA 2 s in glucose-induced insulin secretion is reflected by the fact that secretion is impaired by suppressing their expression or by their pharmacologic inhibition [33,34]. Bacterial infection can lead to the impairment in insulin secretion [21] but the system(s) responsible of this effect has not been established. Attractive candidates are the PLA 2 s because their activity during insulin release by b cells.…”

“…A case of acute cholecystitis and bacteremia with methicillin-resistant Staphylococcus aureus (MRSA) in a patient with HIV infection has been reported and highlights the invasive nature of staphylococcal infections [20]. Moreover, a study on obese mongrel dogs demonstrated that Staphylococcus intermedius infection leads to impaired insulin secretion [21]. S. aureus secretes numerous exotoxins, including a group of polypeptides capable of damaging the host cell plasma membrane.…”

Exendin-4 improves resistance toListeria monocytogenesinfection in diabetic db/db mice

“…Overrepresented dog leukocyte antigen gene influences the type 1 diabetes expression, especially on Samoyed dogs and Miniature Poodles [16,31]. Companion animals eat energy-dense diets that induce obesity-related hyperglycemia and impaired glucose tolerance which in turn increase the risk of infection [21,31,37]. …”