Not exact matches
Friedman's
group was able to track down the mutation in the
obese mice and found that it blocked production
of a particular protein hormone, which they named leptin.
Scientists reached this conclusion by transferring microbes from bypass - treated
obese mice to a
group of lean
mice raised in sterile conditions that left them with no intestinal bacteria at all.
Both
groups became
obese and developed a
mouse form
of diabetes.
Separate
groups of germfree
mice were colonized with uncultured fecal microbiota from each member
of four twin pairs discordant for obesity or with culture collections from an
obese (Ob) or lean (Ln) co-twin.
We examined six experimental
groups of 20 - week - old C57BL / 6J
mice: (a) lean C57BL / 6J female
mice, (b) lean C57BL / 6J male
mice, (c) moderately
obese C57BL / 6J male
mice with diet - induced obesity, (d) moderately
obese female B6.Cg Ay / +
mice, (e) severely
obese female B6.V Lepob / ob
mice, and (f) severely
obese male B6.V Lepob / ob
mice.
Over an eight - week period, a control
group of mice fed a high - fat diet predictably became
obese, but the
mice whose Hedgehog pathway had been activated didn't gain any more weight than another control
group fed on a normal diet.
Obese mice that ate a high - fat diet along with the green tea compound EGCG (Epigallocatechin -3-gallate) gained weight significantly more slowly compared to a control
group of mice which didn't get the green tea supplement.
The final
group, the
obese mice with an inability to create myostatin remained fat, but they also exhibited perks
of their new ability — they were much stronger than their counterparts and their heart and metabolic health had improved.