Other studies have demonstrated that microbes implanted
from lean mice into overweight mice caused the mice to lose weight.
Moreover, obese - phenotype mice were invaded by members of the Bacteroidales
from the lean mice, but, happily, the lean animals resisted invasion by the obese microbiota.
Protective antibodies
from lean mice also failed to protect obese mice from flu infections.
In the second group, they colonized the intestines with flora
from a lean mouse.
Not exact matches
To find out what was going on in the microbiomes of four sets of differently shaped identical twins, researchers transferred some gut bacteria
from a
lean (human) twin to a sterile
mouse: one with no foreign bacteria at all.
The
mouse stayed
lean, even when they later added some bacteria
from the obese twin.
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.
In another animal microbiome experiment, Jeffrey Gordon, a biologist at Washington University in St. Louis, took a suite of microbes
from the guts of both obese and
lean mice and transplanted them into the guts of microbe - free
mice.
«The nondigestible compounds in the Granny Smith apples actually changed the proportions of fecal bacteria
from obese
mice to be similar to that of
lean mice,» Noratto said.
«This is the first study to show that current strategies to bolster the effectiveness of flu vaccines protected
lean mice from serious illness but fell short of protecting obese
mice from infections,» said corresponding author Stacey Schultz - Cherry, Ph.D., a member of the St. Jude Department of Infectious Diseases.
In addition,
lean mice who received vaccines with adjuvants were protected
from severe flu infections.
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.
The researchers used electron microscopy and other imaging techniques to view thousands of cells
from the liver tissue of
lean and obese
mice.
Based on the observation that obese
mice, rats, and humans all had elevated serum concentrations of a protein called GDF15 compared to
lean controls, Yumei Xiong and colleagues set out to develop therapies derived
from the molecule.
The
mice who got microbes
from the
lean twins stayed
lean, the researchers report today in Science.
Microbes
from lean people protect
mice from excessive weight gain, even when animals eat a high - fat, low - fiber diet.
This is interesting, given that muscle /
lean muscle mass ratios of non-skeletal muscle organs
from IL - 15Rα — KO
mice, such as the heart, spleen, and kidneys, were not significantly different
from those of B6129 controls.
Normally, germ - free
mice exposed to a
mouse with microbial - based obesity would themselves become obese, but we could design a microbial community taken
from lean people that protected against this weight gain.
We estimate that the percentage of macrophages in adipose tissue ranges
from under 10 % in
lean mice and humans to over 50 % in extremely obese, leptin - deficient
mice and nearly 40 % in obese humans.
However, when these organ weights were normalized to
lean muscle mass, the organ /
lean muscle mass ratios were not significantly different
from B6129 control
mice (Figure 4, F — H).
Immunohistochemical detection of cells expressing the macrophage - specific antigen F4 / 80 (arrows) in extensor digitalis longus muscles
from C57BL / 6J (a and c) Lepob / ob female and (b and d)
lean female
mice.
We calculated the average adipocyte cross-sectional area and the percentage of F4 / 80 - expressing cells in the perigonadal, perirenal, mesenteric, and subcutaneous inguinal adipose tissue depots
from Ay / + female, Lepob / ob female,
lean male, and diet - induced obese (DIO) male
mice.
The knee cartilage of obese
mice who ate the oligofructose supplement was indistinguishable
from that of the
lean mice.
In one study, researchers took microbiome samples
from both
lean and obese
mice and placed them in the gut of neutral
mice.
The
mice that got their protein
from shellfish became slimmer, despite their fat - and sugar - rich diet, and did not lose
lean body mass either.
Transplanting gut flora
from obese
mice into
lean mice turned the formerly
lean mice fatter... Compelling evidence that gut flora has an important connection to body fat levels.
Additionally, fecal transplant of gut microbes
from obese
mice to GF
mice results in greater adiposity in the GF recipients than fecal transplants
from lean donors (2).
Researchers at Washu took identical twins where one was
lean and other was obese, same genetic material transplanted the microbes into germ - free
mice, and lo and behold, the
mouse who received the microbes
from the obese twin gained weight without any change in diet.
Actually, the leucine - deprived
mice showed no difference in
lean mass,
from either the control
mice or those that were restricted to the same number of (reduced) calories consumed by the leucine - deprived
mice.
However — and this part is miraculous — when Dr. Panda and his team restricted the time the
mice were fed the exact same crappy diet to 12 hours (instead of allowing them to eat whenever they wanted), none of the negative health benefits occurred; the Time - Restricted Fed
mice were 70 %
leaner, lived longer and were free
from diabetes or heart disease.
To explore whether this was a cause of obesity or the effect of it, another research team gave
mice the bacteria
from sets of twins where one was obese and the other was
lean.
Astonishingly, when germ - free
mice are colonized with the gut microbiota
from genetically obese
mice (ob / ob), the otherwise
lean mice dramatically increase body weight.
The
mice that got the bacteria
from the obese people gained weight, while
mice that received bacteria
from the
lean people didn't.
And wait we do; despite the
lean ninety - minute runtime, Downrange can't quite figure out enough variations on their cat - and -
mouse situation to keep the final two acts
from devolving into a boring slog.