the diet, it was spending less to make new proteins,” Brigham
Young University biochemistry professor and senior author,
John Price, said to ALN.
Price cautions that not to expect that restricting calories
will mean that you will stay forever young. There is still a
lot to learn about this process. However, this study forms an
important first step.
“The number one risk factor for most diseases is our age.
The puzzle is: we are born and die with the same genes, so
we know that the time dependent changes in our bodies are
not really due to the genes,” he concluded. “We think that
age is tied to our ability to control the quality of gene products (proteins) in our cells. The goal of this research is to
identify the biochemical mechanisms that drive aging. If we
can identify these processes, we may be able to intercede and
prevent the development of age-related diseases like frailty,
neurodegeneration, and cancer.”
RESVERATROL SHOWS PROMISE AS DIABETES TREATMENT IN
A new study showed that fecal transplants from laboratory
mice fed resveratrol normalized blood sugar in obese mice.
This research, published in the journal Diabetes, could lead
to new treatments for diabetes.
Although previous research indicated that resveratrol, a
natural phenol produced by many plants including grapes and
blueberries, lowered blood sugar levels in obese people, scientists were unsure how exactly it worked because the amount of
resveratrol circulating the blood stream was very low.
“The vast majority of resveratrol does not get absorbed into
the bloodstream and much of it is found in the intestines.
This led us to think that there might be a connection where
resveratrol interacts with intestinal bacteria and wonder if
that is how it has a beneficial effect for diabetes,” Jason
Dyck, professor of pediatrics at the University of Alberta, told
To investigate whether this was true, the research team first
fed resveratrol to obese mice over a period of six weeks. This
altered the rodents microbiome to improve glucose tolerance.
In a second experiment, the team gave obese mice with insulin resistance fecal transplants from healthy laboratory mice
who had been fed resveratrol for 8 weeks.
The results were striking. Within two weeks, the blood
sugar levels of the obese, pre-diabetic mice were almost back
Dyck believes this dramatic change was caused by an
unknown metabolite found in the fecal matter. He and his
team are currently working on determining what exactly this
unknown compound is, with the hopes of using it to develop
a treatment for diabetes.
“Maybe we've identified something that originates from res-
veratrol. Maybe the intestines and intestinal biota turn resver-
atrol into a new metabolite. Maybe resveratrol stimulates the
bacteria to secrete something they don't usually secrete,” Dyck
concluded. “If we can identify and test that one molecule,
maybe that will become an advanced therapy for diabetes.”
JUMPING GENES SUSPECTED IN ALZHEIMER'S DISEASE
The latest round of failed drug trials for Alzheimer’s has researchers
questioning the reigning approach to
battling the disease, which focuses on
preventing a sticky protein called amyloid from building up in the brain.
Duke University scientists have identified a mechanism in
the molecular machinery of the cell that could help explain
how neurons begin to falter in the initial stages of Alzheimer’s,
even before amyloid clumps appear.
This rethinking of the Alzheimer’s process centers on human
genes critical for the healthy functioning of mitochondria, the
energy factories of the cell, which are riddled with mobile
chunks of DNA called Alu elements.
If these “jumping genes” lose their normal controls as a
person ages, they could start to wreak havoc on the machinery
that supplies energy to brain cells—leading to a loss of neurons
and ultimately dementia, the researchers say.
In Alzheimer’s patients, the thinking goes, the mitochondria
in neurons stop working properly. As a result they are unable
to generate as much energy for neurons, which starve and die
with no way to replenish them. But how mitochondria in neurons decline with age is largely unknown.
Most mitochondrial proteins are encoded by genes in the cell
nucleus before reaching their final destination in mitochondria.
In 2009, Duke neurologist and study co-author Allen Roses
identified a non-coding region in a gene called TOMM40 that
varies in length. Roses and his team found that the length of
this region can help predict a person’s Alzheimer’s risk and
age of onset.
Larsen wondered if the length variation in TOMM40 was
only part of the equation. He analyzed the corresponding gene
region in gray mouse lemurs, teacup-sized primates known
to develop amyloid brain plaques and other Alzheimer’s-like
symptoms with age. He found that in mouse lemurs alone, but
not other lemur species, the region is loaded with short stretch-es of DNA called Alus.
Found only in primates, Alus belong to a family of retro-transposons or “jumping genes,” which copy and paste themselves in new spots in the genome. If the Alu copies present
within the TOMM40 gene somehow interfere with the path
from gene to protein, Larsen reasoned, they could help explain
why mitochondria in nerve cells stop working.
The TOMM40 gene encodes a barrel-shaped protein in the
outer membrane of mitochondria that forms a channel for
molecules—including the precursor to amyloid—to enter.
Larsen used 3D modeling to show that Alu insertions within
the TOMM40 gene could make the channel protein it encodes
fold into the wrong shape, causing the mitochondria’s import
machinery to clog and stop working.