It appears that even high fat diet, HDF, a modern day culinary and medical villain, has a positive characteristics, at least one we know of.
This is what a new paper in journal Nature suggests. This research, led by Thirumala-Devi Kanneganti at St. Jude Children's Research Hospital, Memphis, studied mice with Pstpip2 mutation that spontaneously develop bone inflammation and bone erosion.
Surprisingly, the authors reported that these mutant mice when fed with high fat diet, but not regular low fat diet, showed no sign of bone inflammation.
The authors found that there was a correlation between the disease progression and abundance of gut flora microbe Prevotella.
Interestingly, high fat diet could reduce the abundance of Prevotella in Pstpip2 mutant mice, implying that diet-induced alteration in gut flora contributed to disease protection.
Indeed, antibiotic treatment of Pstpip2 mutant mice could dramatically reduce disease development.
Alternatively, transplantation of fecal microbiota from HFD-fed Pstpip2 mice, but not low fat diet-fed Pstpip2 mice, into young Pstpip2 mice could prevent development of bone inflammation.
Mechanistically, HFD beneficial effect on bone inflammation was related to the reduction of IL-1beta production in HFD-fed Pstpip2 mice.
Finally, the authors showed that antibody depletion of neutrophils could prevent bone erosion and inflammation in Pstpip2 mice.
In summary, the authors proposed that diet-induced gut flora modification alters IL-1beta mediated inflammatory bone damage in Pstpip2 mice.
HFD is usually shown to have a negative effect on metabolic syndrome, on development of type II diabetes, for example. The results in this paper are exception to this rule. Interestingly, Pstpip2 mice did not gain weight on HFD diet, implying that thermo-regulation and energy expenditure is differently regulated in Pstpip2 mice. Is there any role of innate lymphoid cell type 2, ILC2?