Alzheimer's disease thought to be accelerated by an abnormal build-up of fat in the brain

The researchers examined the brains of nine patients who died from Alzheimer's disease and found significantly more fat droplets compared with five healthy brains. A team of chemists from University of Montreal led by Pierre Chaurand then used an advanced mass spectrometry technique to identify these fat deposits as triglycerides enriched with specific fatty acids, which can also be found in animal fats and vegetable oils.
"We discovered that these fatty acids are produced by the brain, that they build up slowly with normal aging, but that the process is accelerated significantly in the presence of genes that predispose to Alzheimer's disease"



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Activation and repression of Epstein-Barr virus and Kaposi sarcoma-associated herpesvirus lytic cycles by short- and medium-chain fatty acids.

The lytic cycles of Epstein-Barr virus (EBV) and Kaposi
sarcoma-associated herpesvirus (KSHV) are induced in cell culture by
sodium butyrate (NaB), a short-chain fatty acid (SCFA) histone
deacetylase (HDAC) inhibitor. Valproic acid (VPA), another SCFA and HDAC
inhibitor, induces the lytic cycle of KSHV, but blocks EBV lytic
reactivation. To explore the hypothesis that structural differences
between NaB and VPA account for their functional effects on the two
related viruses, we investigated the capacity of 16 structurally related
short- and medium-chain fatty acids to promote or prevent lytic cycle
reactivation. SCFAs differentially affected EBV and KSHV reactivation.
KSHV was reactivated by all SCFAs that are HDAC inhibitors, including
phenylbutyrate. However, several fatty acid HDAC inhibitors, such as
isobutyrate and phenylbutyrate, did not reactivate EBV. Reactivation of
KSHV lytic transcripts could not be blocked completely by any fatty acid
tested. In contrast, several medium-chain fatty acids inhibited lytic
activation of EBV. Fatty acids that blocked EBV reactivation were more
lipophilic than those that activated EBV. VPA blocked activation of the
BZLF1 promoter by NaB, but did not block the transcriptional function of
ZEBRA. VPA also blocked activation of the DNA damage response that
accompanies EBV lytic cycle activation. Properties of SCFAs in addition
to their effects on chromatin are likely to explain activation or
repression of EBV. We conclude that fatty acids stimulate the two
related human gamma-herpesviruses to enter the lytic cycle through
different pathways.

IMPORTANCE:

Lytic reactivation of EBV
and KSHV is needed for persistence of the virus and plays a role in
carcinogenesis. Our direct comparison highlights the mechanistic
differences of lytic reactivation between related human oncogenic
gammaherpesviruses. Our findings have therapeutic implications, as fatty
acids are found in the diet and produced by human microbiota. Small
molecule inducers of the lytic cycle are desired for oncolytic therapy.
Inhibition of viral reactivation, alternatively, may prove useful in
cancer treatment. Overall, our findings contribute to understanding
pathways that control the latent to lytic switch and identify naturally
occurring molecules that may regulate this process.

Polyunsaturated fatty acid saturation by gut lactic acid bacteria affecting host lipid composition

In the representative gut bacterium Lactobacillus plantarum, we identified genes encoding the enzymes involved in a saturation metabolism of polyunsaturated fatty acids and revealed in detail the metabolic pathway that generates hydroxy fatty acids, oxo fatty acids, conjugated fatty acids, and partially saturatedtrans-fatty acids as intermediates. Furthermore, we observed these intermediates, especially hydroxy fatty acids, in host organs. Levels of hydroxy fatty acids were much higher in specific pathogen-free mice than in germ-free mice, indicating that these fatty acids are generated through polyunsaturated fatty acids metabolism of gastrointestinal microorganisms. These findings suggested that lipid metabolism by gastrointestinal microbes affects the health of the host by modifying fatty acid composition.

New Epilepsy Drug From Fatty Acids

Scientists in London have identified specific fatty acids that could form the basis of new drugs to treat epilepsy in children and adults. They suggest drugs based on them could provide similar epilepsy control as a ketogenic diet, a treatment often prescribed for children with severe drug-resistant epilepsy and which mimics aspects of starvation but with troubling side effects.

How Dietary Fat Regulates Cholesterol Absorption

Their findings suggest a tightly regulated system in which cholesterol is only taken up by the intestine in the presence of fats. One reason such regulation is important, Dr. Walters said, is that unprocessed cholesterol can be toxic to cells and requires fatty acid-mediated modification to render it safe in a process called esterification.The most effective was oleic acid (derived from olive oil)