In the same study, a concomitant treatment of fructose-fed mice with non-resorbable antibiotics (polymyxin B and neomycin), resulting in a reduction of fecal bacteria of >99%, attenuated the development of liver steatosis and inflammatory alterations in mice 51, suggesting that mechanism underlying the effects of fructose with respect to MASLD development may go beyond the insulin independent (and somewhat faster) metabolism of the monosaccharide (see below). The gene discussed is INS; the disease is metabolic dysfunction-associated steatotic liver disease.