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Chemistry (including Biochemistry)/Biochemical mechanism: fat to cellular energy

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I am a college student taking a basic nutrition course. My (very slight) biochem background has caused me to find a question that is outside the scope of the course. Google and AskScience on Reddit have yielded no results, and I'm convinced I am misunderstanding some basic principle.

My assumptions are:
1) Glucose is the preferred method of energy intake by the cell.
2) Glucose is formed by either (a) the breakdown of carbohydrates, or (b) the breakdown of previously stored fat.
3) If (b), the breakdown of fats into glucose causes ketone bodies to form, which can lead to ketosis, a toxic build up of ketone bodies.
4) People are capable of losing weight without poisoning themselves to death.

My questions are:
1) How do people use their own fat stores for energy if the body's method of preparing those fat stores for cellular energy use causes toxic ketone buildup?
2) If fat can be used directly for energy, why does the body ever choose to convert it to glucose if that method is poisonous?
3) What are the various biochemical pathways that the body uses for energy if there is a currency beyond glucose? In other words, on a chemical level, what forms of energy can a cell use, how does it work, and what are the benefits and disadvantages of each type of energy use?

Thank you!

Answer
What Feeds Cellular Respiration
What Feeds Cellular Re  
Hello Amber!

The process you're curious about is called cellular respiration. While it is true that glucose is a cell's favorite fuel, it is not the only fuel a cell can use. Please bear with me for a few moments, as you have asked a long question with many differing players.

There are three main processes in cellular respiration; glycolysis, the citric acid cycle, and oxidative phosphorylation.

Glycolysis breaks down sugar in a reaction to make ATP (cellular energy molecule, kind of like a rechargeable battery), pyruvate, and NADH (mitochondria batteries). This is not the world's most efficient way to make ATP because it occurs in the cellular water of the cell between organelles. Biochemistry's best reactions usually occur by passing atoms across cellular membranes. Oxidative phosphorylation in the mitochondria is a great example of this, where mitochondria use proteins in their inner membrane. These take NADH and use it to power cellular machines that make a huge amount of ATP from ADP... which is a cell's favorite fuel to help unfavorable reactions go.

Helpfully, glycolysis is not the only source of NADH - the major source of that takes place inside the mitochondria, and is called the citric acid cycle. The citric acid cycle can be likened to the currency exchange desk at international airports - the cell can put a number of different reactants into the citric acid cycle and still get energy out the other end. So the pyruvate that was made in glycolysis can be broken down here, as can ketones made by breaking down fatty acids. Someone on an extremely high protein diet can use the TCA cycle to take amino acids (protein monomers) and make energy from those, too. Alternately, the cell can repurpose molecules acquired in the diet through the TCA cycle enzyme workshop to build other structures as needed.

In short, the molecules the cell can use to feed cellular respiration can be found in this figure. (Must copy and paste link into browser input bar at top of page if image attachment does not work.)
https://ka-perseus-images.s3.amazonaws.com/16eb9b45c81ecf239789608beef4dbdc033a0415.png

A good introduction to cellular respiration can be found in most contemporary not-for-majors biology books. I do cover this material in biology classes I teach to majors as well as biology nonmajors. If most of what I said up above looks like technobabble nonsense, then I'd suggest sitting down with your favorite beverage and watching this video series online. Episode six deals with cellular respiration in detail with good humor.

https://www.youtube.com/playlist?list=PLwL0Myd7Dk1F0iQPGrjehze3eDpco1eVz (Alt: google Amoeba Sisters Biology Videos in Sequence.)

To address some of your more specific questions:

I notice you assume that ketones are always toxic, but this is not so. The body has scavenging mechanisms to turn ketones into energy. As it says on Wikipedia (https://en.wikipedia.org/wiki/Ketone_bodies)

<em>"The heart preferentially utilizes fatty acids for energy under normal physiologic conditions. However, under ketotic conditions, the heart can effectively utilize ketone bodies for energy" </em>

So heart cells would rather 'eat' fat, but can eat ketones too by using the citric acid cycle. This may be because the blood level of glucose can spike and drop, but there will always be fat cells for the using.

Like many things, the body can also simply urinate extra unused ketones out, or get rid of them in other ways. Ever notice how low-blood-sugar diabetics have stinky breath? They are exhaling extra ketones that the brain uses to keep going. For normal healthy folks, the switch from a sugar powered brain to a ketone powered brain happens during fasting and is no big deal. Ketones are only toxic in unusual circumstances when cellular metabolism is unbalanced. (ex: diabetes. Most often in diabetes cells cannot get sugar from the bloodstream, and so are 'stuck' breaking down fat to survive.)

So ultimately when we lose extra mass (fat molecules) where do the carbons go? We exhale them - the end products of cellular respiration are water, many recharged ATP, and carbon dioxide.

Hopefully this helps - in reality, people can and do write books to answer this question! You can also check out Khan Academy to help you understand what is going on.

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Trista Robichaud, PhD

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No homework questions, especially ones copied and pasted from textbooks. I will answer questions about principles or give hints, but I do not do other's homework. I'm comfortable answering basic biochemistry, chemistry, and biology questions up to and including an undergraduate level of understanding. This includes molecular biology, protein purification, and genetics. My training/inclination is primarily in structural biology, or how the shapes of things affect their function. Other interests include protein design, protein engineering, enzyme kinetics, and metabolic diseases such as cancer, atherosclerosis, and diabetes. My chemistry weaknesses are that I do not know organic or inorganic synthesis well, nor am I familiar with advanced inorganic reactions. I will attempt quantum mechanics and thermodynamics questions, but primarily as they relate to biological systems. Furthermore, I cannot tell you if a skin photograph is cancerous, or otherwise diagnose any disease. I can tell you how we currently understand the basic science behind a disease state, but I cannot recommend treatment in any way. Please direct such questions to your medical professional.

Experience

I hold a PhD in Biomedical Science from the University of Massachusetts Medical School in Worcester. I specialize in Biochemistry, with a focus on protein chemistry. My thesis work involved the structure and functions of the human glucose transporter 1. (hGLUT1) Currently I am a postdoc working in peptide (mini-protein) design and enzymology at the University of Texas Health Science Center in San Antonio, Texas. I am in Bjorn Steffensen's lab (PhD, DDS), studying gelatinase A and oral carcinoma.

Organizations
2001 American Association for the Advancement of Science
2007 American Chemical Society
2007 Protein Society
2011 UTHSCSA Women’s Faculty Association


Publications
Levine KB, Robichaud TK, Hamill S, Sultzman LA, Carruthers A. Properties of the human erythrocyte glucose transport protein are determined by cellular context. Biochemistry 44(15):5606-16, 2005. (PMID 15823019)
Robichaud TK, Appleyard AN, Herbert RB, Henderson PJ, Carruthers A “Determinants of ligand binding affinity and cooperativity at the GLUT1 endofacial site” Biochemistry 50(15):3137-48, 2011. (PMID 21384913)
Xu X, Mikhailova M, Chen Z, Pal S, Robichaud TK, Lafer EM, Baber S, Steffensen B. “Peptide from the C-terminal domain of tissue inhibitor of matrix metalloproteinases-2 (TIMP-2) inhibits membrane activation of matrix metalloproteinase-2 (MMP-2)” Matrix Biol. 2011 Sep;30(7-8):404-12. (PMID: 21839835)
Robichaud TK, Steffensen B, Fields GB. Exosite interactions impact matrix metalloproteinase collagen specificities. J Biol Chem. 2011 Oct 28;286(43):37535-42 (PMID: 21896477)

Poster Abstracts:
Robichaud TK, Carruthers. A "Mutagenesis of the Human type 1 glucose transporter exit site: A functional study." ACS 234th Meeting, Boston MA. Division of Biological Chemistry, 2007
Robichaud TK, Bhowmick M, Tokmina-Roszyk D, Fields GB “Synthesis and Analysis of MT1-MMP Peptide Inhibitors” Biological Chemistry Division of the Protein Society Meeting, San Diego CA 2010
Robichaud TK; Tokmina-Roszyk D; Steffensen B and Fields GB “Catalytic Domain Exosites Contribute to Determining Matrix Metalloproteinase Triple Helical Collagen Specificities” Dental Science Symposium. UTHSCSA 2011
Robichaud TK; Tokmina-Roszyk D; Steffensen B and Fields GB “Exosite Interactions Determine Matrix Metalloproteinase Specificities” Gordon Research Conference on Matrix Metalloproteinase Biology, Bristol RI 2011


Education/Credentials
Oakland University, Auburn Hills MI BS, Biochemistry 1998
University of Massachusetts Medical School, Worcester MA PhD, Biochemistry & Molecular Pharmacology 2001-2008
University of Texas Health Science Center, San Antonio TX Postdoc, Biochemistry 2009-Present


Awards and Honors
1998 Honors College Graduate, Oakland University
2009 Institutional National Research Service Award, Pathobiology of Occlusive Vascular Disease T32 HL07446
2011 1st Place, Best Postdoctoral Poster, Dental Science Symposium, UTHSCSA, April 2011


Past/Present Clients
Invited Seminars:
Robichaud TK, Fields GB. “Synthesis and Analysis of MTI-MMP Triple Helical Peptide Inhibitors” Pathology Research Conference, University of Texas Health Science Center San Antonio Pathology Department (June 18th, 2010)
Robichaud TK & Hill, B “How To Give A Great Scientific Talk” Invited Lecture, Pathobiology of Occlusive Vascular Disease Seminars, UTHSCSA (Nov 11th 2010), Cardiology Seminar Series, Texas Research Park (Feb 21st, 2011)
Robichaud TK; Tokmina-Roszyk D; Steffensen B and Fields GB “Exosite Interactions Determine Matrix Metalloproteinase Specificities” Gordon-Keenan Research Seminar “Everything You Wanted to Know About Matrix Metalloproteinases But Were Afraid to Ask” Bristol, RI (Aug 6th, 2011)

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