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  #1   ^
Old Sun, Feb-26-17, 11:28
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WereBear WereBear is offline
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Default Overeating is Bad for Mitochondria: Calories Count

Here's another timely post by Dr. Cate:

Quote:
Overeating is Bad for Mitochondria: Calories Count

There’s a lot of important discussion around macronutrients in the nutrition world regarding what percentage of our daily calories should ideally come from protein versus carb versus fat. In all this discussion, what’s often overlooked is the fact that simply overeating puts a stress on the system.

I think we should include a fourth macronutrient: time between meals.


There's lots of fascinating stuff here, including a video. It supports the ideas behind Intermittent Fasting and only eating to hunger, plus lots more:

Quote:
This 15 minute youtube lecture below provides a fundamental insight to what overeating does to our metabolism. In order to understand the true origin of insulin resistance and other diseases of overconsumption we must look inside mitochondria. Mitochondria are the battery packs powering most of life on Earth including our brain and muscle cells. It turns out most of us have been overstuffing these little guys with too much energy, and now we know that doing so can harm them.

Dr. P. Darrel Neufer explains how a mitochondria works like a battery. We literally charge mitochondria with electrons when we eat, and drain those electrons with activity that moves protons through the pump. The problems arise when we over charge our batteries. Unlike real batteries, which simply ignore the charge and the electrical balance inside our house is unaffected, our mitochondria must disrupt our body’s hormonal balance in order to protect themselves.


Amazing stuff. Like they say, read the whole thing.
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  #2   ^
Old Sun, Feb-26-17, 12:24
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http://onlinelibrary.wiley.com/doi/...08.05460.x/full

Quote:
Abstract

The ketogenic diet (KD) is a high-fat, low carbohydrate diet that is used as a therapy for intractable epilepsy. However, the mechanism(s) by which the KD achieves neuroprotection and/or seizure control are not yet known. We sought to determine whether the KD improves mitochondrial redox status. Adolescent Sprague–Dawley rats (P28) were fed a KD or control diet for 3 weeks and ketosis was confirmed by plasma levels of β-hydroxybutyrate (BHB). KD-fed rats showed a twofold increase in hippocampal mitochondrial GSH and GSH/GSSG ratios compared with control diet-fed rats. To determine whether elevated mitochondrial GSH was associated with increased de novo synthesis, the enzymatic activity of glutamate cysteine ligase (GCL) (the rate-limiting enzyme in GSH biosynthesis) and protein levels of the catalytic (GCLC) and modulatory (GCLM) subunits of GCL were analyzed. Increased GCL activity was observed in KD-fed rats, as well as up-regulated protein levels of GCL subunits. Reduced CoA (CoASH), an indicator of mitochondrial redox status, and lipoic acid, a thiol antioxidant, were also significantly increased in the hippocampus of KD-fed rats compared with controls. As GSH is a major mitochondrial antioxidant that protects mitochondrial DNA (mtDNA) against oxidative damage, we measured mitochondrial H2O2 production and H2O2-induced mtDNA damage. Isolated hippocampal mitochondria from KD-fed rats showed functional consequences consistent with the improvement of mitochondrial redox status i.e. decreased H2O2 production and mtDNA damage. Together, the results demonstrate that the KD up-regulates GSH biosynthesis, enhances mitochondrial antioxidant status, and protects mtDNA from oxidant-induced damage.


This doesn't take away from the idea of calorie moderation entirely, a diet with a given ketogenic ratio becomes less ketogenic with increased intake. Also, ketogenic and control diets were calorie restricted to 90 percent of ad lib intake.

This is shown by bar graph, so hard to say precisely, but hippocampal lipoic acid levels looks like about 2 ng/g tissue for the control diet, 14 ng/g tissue for the ketogenic diet, wow.
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Old Tue, Feb-28-17, 05:24
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https://www.sciencedaily.com/releas...70223102558.htm

I think this makes sense here, it's a study looking at mitochondrial stress and diabetic kidney disease.


Quote:

Diabetic kidney disease is decoded, offering new avenues for diagnosis and treatment

Diabetes is a leading cause of kidney disease, a serious, often fatal complication that is difficult to diagnose in early, potentially treatable stages. Now, a research team at the Icahn School of Medicine at Mount Sinai has revealed biological pathways involved in diabetic kidney disease, providing hope that both early diagnostic tests and targeted treatment can be designed.

The study, published in Diabetes, shows that oxidative stress in the "power plants" within a population of kidney cells progressively impairs the ability of the bean-shaped organs to strain blood for waste products and produce urine. The research team also found a cellular receptor that can be blocked to modulate that stress reaction. Blocking that receptor saved the kidneys in mice genetically destined to develop diabetic kidney failure.

About 30 percent of patients with type 1 (juvenile onset) diabetes and 10 to 40 percent of those with type 2 (adult onset) diabetes eventually will suffer from kidney failure, according to the National Kidney Foundation. When that happens, patients must turn to dialysis or kidney transplantation, if available.

"Diabetic kidney disease is one of the major causes of death in diabetic patients, and is also the leading single cause of end-stage renal disease in the United States," says the study's senior investigator, Ilse S. Daehn, PhD, Assistant Professor of Medicine (Nephrology) at the Icahn School of Medicine at Mount Sinai. "Our findings open new diagnostic opportunities for early detection and potential therapeutic strategies to protect against further renal damage in patients."

The study's findings essentially offer a "fundamental paradigm shift in our understanding of the development and treatment of diabetic kidney disease," says Dr. Daehn, who is also a member of The Charles Bronfman Institute for Personalized Medicine.

Investigators focused on the kidney's glomerulus -- globular bodies, full of capillaries and other structures, that serve as the first stage and the key unit in the filtration of blood for waste products to be expelled in urine.

The research team studied three different cell types that interact within the glomerulus, using two sets of mice. One group naturally develops diabetic kidney disease and the other group is naturally resistant to the disorder.

They discovered that in mice prone to kidney disease, endothelial cells were affected. In these wafer-like cells, which form the inner lining of blood vessels, the mitochondria -- cellular subunits that act like power plants, producing energy -- were stressed, and so made excess amounts of reactive oxygen species (ROS). These are molecules that have important roles in cell signaling but, when overproduced, can damage cell proteins and DNA.

This process begins to destroy podocytes, cells that wrap around and work with capillaries and the other cell types in the glomerulus. The glomerulus eventually becomes brittle, the capillaries collapse, and kidneys become leaky, shedding essential body proteins. Progressive damage leads to kidney failure, resulting in end-stage kidney disease.

The research team was able to measure, in susceptible mice, molecules linked to excess ROS, suggesting that a biomarker could be developed that signals early development of kidney disease in humans. And knowing that ROS excess leads to kidney disease implies that agents that collect ROS molecules within the kidney might provide a potential therapy, Dr. Daehn says.

Investigators then looked for "upstream" regulators of mitochondrial stress within the endothelium in the glomerulus and discovered a pathway that helps manage this oxidative stress. This pathway produced excess quantities of a cell receptor, endothelium receptor-A, as well as its ligand -- the protein that binds to the receptor.

This discovery means that a small molecule that blocks the ligand from binding to its receptor might tamp down production of mitochondrial ROS, thus halting damage to the glomerulus, Dr. Daehn says.

The researchers used an experimental small molecule, BQ-123, to specifically block this receptor and found that mice that were destined to develop diabetic kidney disease were spared from the disorder.

Researchers tested their hypothesis by looking at urine and kidney biopsies from patients with diabetic kidney disease. They found molecules in the urine linked to oxidative stress and rapid disease progression, and biopsies that showed increased mitochondrial DNA damage and increased endothelium receptor-A expression.

"These findings in human samples go a long way to substantiate our hypotheses, which is exciting because it represents a new way forward to understanding and treating diabetic kidney disease," Dr. Daehn says.


This fits with Charles Mobbs's observation of kidney disease reversal in mice with a ketogenic diet. There are studies showing reduced oxidative stress with a ketogenic diet (my last post in this thread is an example). Also, that "endothelium receptor-A;"

Quote:
ETA is a subtype for vasoconstriction[1] These receptors are found in the smooth muscle tissue of blood vessels, and binding of endothelin to ETA increases vasoconstriction (contraction of the blood vessel walls) and the retention of sodium, leading to increased blood pressure


is another possible connection, given that ketogenic diets tend to decrease sodium retention and decrease blood pressure.


Protein restriction is the most mainstream dietary prescription vs. kidney disease, and even there, there is a connection to mitochondrial reactive oxygen species.

Quote:
Dietary protein restriction decreases oxidative protein damage, peroxidizability index, and mitochondrial complex I content in rat liver.
Ayala V1, Naudí A, Sanz A, Caro P, Portero-Otin M, Barja G, Pamplona R.
Author information
Abstract
Caloric restriction (CR) decreases oxidative damage, which contributes to the slowing of aging rate. It is not known if such decreases are due to calories themselves or specific dietary components. In this work, the ingestion of proteins of Wistar rats was decreased by 40% below that of controls. After 7 weeks, the liver of the protein-restricted (PR) animals showed decreases in oxidative protein damage, degree of membrane unsaturation, and mitochondrial complex I content. The results and previous information suggest that the decrease in the rate of aging induced by PR can be due in part to decreases in mitochondrial reactive oxygen species production and DNA and protein oxidative modification, increases in fatty acid components more resistant to oxidative damage, and decreased expression of complex I, analogously to what occurs during CR. Recent studies suggest that those benefits of PR could be caused, in turn, by the lowered methionine intake of that dietary manipulation.
PMID: 17452727
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  #4   ^
Old Tue, Feb-28-17, 07:58
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Mitochondrial health is the new breakthrough, it seems.

This is a framework which can be adapted to all kinds of new realizations, I am hoping.
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