In a study published in the open access journal BMC Biology, researchers show that its effectiveness against a number of susceptible Lepidopteran species depends on the presence of the normally "friendly" bacteria that colonise their guts. Without these bacteria, the Bt toxin can become impotent in some species.
A team of researchers from the University of Wisconsin studied the effects of wiping out the commensal gut bacteria using antibiotics in six moth and butterfly species. In five of these species, the antibiotic treatment protected the insects against the lethal effects of the toxin, and in four of the five species, replacing the gut bacteria caused the toxin to become effective again. Graduate student Nichole Broderick said, "Our results suggest that Bt may kill some insects by causing otherwise benign gut bacteria to exert pathogenic effects. If the insects don't have these bacteria present, the toxin may be ineffective".
According to the authors, "We've shown that larval enteric bacteria affect susceptibility to Bt, and the extent of this impact varies across butterfly and moth species. This does not exclude other factors, including the insect host, B. thuringiensis strain, and environmental conditions. In some cases these factors may interact, for example, host diet can alter the composition of enteric bacteria".
They conclude, "From a pest management perspective, the ability of a non-specific enteric bacterium to restore B. thuringiensis-induced mortality of some Lepidopteran species may provide opportunities for increasing susceptibility or preventing resistance".
biomedcentral/
Those treatments improved the animals' metabolic profiles by lowering levels of SREBP-1 and other fat-building genes in their livers. The mice also showed a reversal of their fructose-induced insulin resistance and a threefold increase in glucose uptake in their fat tissue.
"These data support an important role for PGC-1b in the pathogenesis of fructose-induced insulin resistance and suggest that PGC-1b inhibition may be a therapeutic target for treatment of NAFLD, hypertriglyceridemia, and insulin resistance associated with increased de novo lipogenesis," the researchers concluded.
The new study has "revealed the transcriptional coactivator PGC-1b as a missing link between fructose intake and metabolic disorders," wrote Carlos Hernandez and Jiandie Lin of the University of Michigan Medical Center, Ann Arbor in an accompanying commentary. "The findings ‚¬?¦support the emerging role of gene/environment interaction in modulating the metabolic phenotype and disease pathogenesis. Thus, perturbations of the same regulatory motif may produce vastly different metabolic responses, depending on the specific combinations of dietary nutrients," they continued.
cellpress/