a summary of how fat burning process works and is activated... - AnabolicMinds.com

a summary of how fat burning process works and is activated...

  1. Enhanced Body Formulations REP
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    a summary of how fat burning process works and is activated...


    Merry Christmas all,

    Since joining a law firm part time as an internship, I have had a couple of people ask me about this topic and as i have no medical or science background, wonder if anyone can help me understand and explain it to others so i can help them. Nutrition wise i am steeped, but not science...

    Thanks guys...

    -Chris
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    Superhumanradio was talking about ketosis/fatloss yesterday and they went into a pretty good description of how fatloss occurs. Maybe they have it archived.
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    Quote Originally Posted by RedwolfWV
    Superhumanradio was talking about ketosis/fatloss yesterday and they went into a pretty good description of how fatloss occurs. Maybe they have it archived.
    Will look for it...show number# ? Thanks bro

    -Chris
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    THE FUTURE OF LEAN
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    I really dont know the show number unfortunatly. Sorry man
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    You are opening up an entire cup of worms. Fat burning during exercise depends on 7 factors:

    • Mobilization
    • Circulation
    • Uptake
    • Activation
    • Translocation
    • β-oxidization
    • Oxidative phosphorylation

    Here's some notes that may help:

    • Mobilization
      • Depends on
        • Lypolysis rate
        • FFA carrying capacity of blood in adipose region (ATBF)
        • Re-esterfication
        • Lactate (inhibits)
      • Adipose tissue blood flow
        • Delivers hormones
        • Delivers fatty acid carrier proteins
        • Carries FA away from adipocytes
      • FFA carrying capacity based upon
        • Albumin concentration
        • Blood flow
        • Free FFA binding sites on albumin
          • When saturated, many FFA are reattached to glycerol
      • Regulation
        • Re-esterification reduces and stores FFA
        • Vascular resistance decreases blood flow to adipocytes
    • Circulation
      • 99.9% FFA in plasma bound to albumin
      • 8-10 binding sites per albumin
        • Low affinity
      • Unbound FFA in circulation is in equilibrium with bound
      • Initial decrease in plasma FFA at onset of exercise
        • Increase in FFA utilization
      • Progressive increase as exercise continues
        • Lypolysis and FFA release increase
      • Increase mediated by
        • Rise in catecholamines
        • Drop in insulin
      • Excessive FFA release in unfit may result in increased release of tryptophan by albumin thus leading to fatigue







    Lipolysis of circulating lipoproteins

    • Lipolysis of TAG within lipoproteins small during exercise
      • Most circulating TAG held in VLDL and chylomicrons
      • TAG inside must be hydrolyzed by LPL attached to capillary endothelium
    • FFA liberated by LPL may be taken up by muscle or adipose
      • Some are released into circulation non-esterfied
    • LPL has higher affinity for chylomicron over VLDL


    Lecture VII: Lipid Metabolism Cont.


    • Uptake
      • Dependent upon plasma levels (push) and FFA oxidization (pull)
        • Not linear relationship
      • Higher turnover during exercise
        • Greater FFA oxidization (pull)
        • Higher plasma concentration via catecholamine stimulation (push)
      • FFA has to pass through 5 spaces to reach mitochondria
        • Microvascular space
        • Endothelium
        • Interstitium
        • Sarcolemma
        • Intramyocytal space
      • FFA are hydrophobic – require protein to travel through blood (albumin)
        • Binding proteins carry FFA across endothelium
      • Tissues contain fatty acid binding proteins to carry across membrane
        • Concentration gradient between extra and intercellular space favors influx
        • Binding proteins translocate from cytoplasm to membrane (similar to glut4) in response to exercise and insulin
        • Also carry FFA to mitochondria
        • As pH decreases rate of dissociation increases
        • FFA use during exercise is limited to delivery
          • Ability to extract FFA from blood
            • Training increases this
      • Only 20-40 mmol/kg of intramuscular TAG is stored
        • During long duration exercise, intramuscular TAG is depleted (to 6-8 mmol) within 2-3 hr
          • Remainder is structural TAG
        • Some FFA uptake during exercise is used to replete intramuscular TAG
          • Ca and cAMP increases intramuscular TAG lipase activity


    [IMG]file:///C:/Users/Jay/AppData/Local/Temp/msohtmlclip1/01/clip_image002.jpg[/IMG]


    • Activation
      • Upon entrance to the cell, FA is attached to CoA forming fatty acyl CoA (acyl CoA synthase)
        • Occurs on outer mitochondrial membrane & ER
        • Requires 2 ATP
    • Translocation – carnitine levels could be limiting in FA oxidization during exercise
      • Carnitine palmitoyultransferase (CPT) transports FA CoA to mitochondria
      • CTP complex: CTPI, Acylcarnitine translocase, CPTIIj
      • CPI transfers fatty acyl groups to carnitine across outer membrane
        • FA CoA CoASH + AcylCarnitine
        • Inhibited by maloynl CoA (FA synthesis intermediate)
      • Acylcarnitine translocase transfers acylcarnitine across inner membrane
      • CPTII splits fatty acyl CoA from carnitine
        • AcylCarn FA CoA + Carn
        • FAl CoA to beta oxidization
        • Carn back to intramembranous space



    [IMG]file:///C:/Users/Jay/AppData/Local/Temp/msohtmlclip1/01/clip_image004.jpg[/IMG]

    • Beta-oxidation
      • FA degrading at the β carbon
        • Carbons labeled right to left
          • Carbon at carboxyl group is 1
          • Beside 1 is α
          • Cleavage occurs between α and β
      • Occurs in mitochondrial matrix
      • Each turn of the cycle shortens the FA by 2 carbons and produces
        • 1 FADH
        • 1 NADH
        • 1 A CoA
      • Hydroxyl CoA dehydrogenase (HOAD) is marker of cells ability to oxidize fat
      • Β-ketothiolase is rate limiting step in beta ox
        • Breaks ketoacyl CoA down into an actyl CoA and a FA CoA



    [IMG]file:///C:/Users/Jay/AppData/Local/Temp/msohtmlclip1/01/clip_image006.jpg[/IMG]
    [IMG]file:///C:/Users/Jay/AppData/Local/Temp/msohtmlclip1/01/clip_image008.jpg[/IMG]


    • Sites of potential FA oxidation control during exercise
      • Adipose lipolysis
      • FFA delivery
      • FFA movement across sarcolemma
      • Regulation of muscle TAG lipase
      • Regulation of FFA movement across mitochondrial membrane


    Here's an excerpt from my dissertation regarding adiposity control.

    Body composition may be improved either by increasing lean body mass or decreasing fat mass. Subcutaneous adipose tissue is the main storage site for TAG. Lipid accumulation in human adipose tissue is determined by the balance between lipogenesis and lipolysis (Ormsbee et al., 2009). For reductions in adiposity to occur lipids must first be mobilized and released from adipose tissue, transported to muscles and/or liver, taken up by the active tissue, activated and translocated into the mitochondria, and then undergo β-oxidation (Brooks et al., 2005a).
    To better understand how betaine may improve body composition by influencing adiposity, the following physiological processes will be reviewed: lipogenesis, lipolysis, and fatty acid translocation.
    Lipogenesis
    Lipogenesis occurs in liver and adipose tissue, and describes a series of processes in fatty acid and TAG synthesis (Perrone et al., 2008). The majority of lipid deposition in adipose tissue is provided by TAG synthesis; however, some is also provided from the formation of fatty acids from glucose via de novo lipogenesis (Hellersteine, 1999). TAG synthesis involves describes the uptake and synthesis of free fatty acids (FFA) into triglycerdies. In brief, FFA are liberated by chylomicrons and very low density lipoproteins via lipoprotein lipase (LPL). Next, FFA enters the adipocyte both passively and via the subcutaneous adipose tissue fatty acid transporter (Bonen, Tandon, Glatz, Luiken, & Heigenhauser, 2006). Intracellular FFA is activated by the attachment of a coenzyme A molecule via aceyl-CoA synthase (ACS), then attached to glycerol 3-phosphate to form monoacylglycerol (Houston, 2006). Finally, monoacylglycerol undergoes two parallel TAG synthetic pathways in the endoplasmic reticulum to form TAG (Shi & Burn, 2004).
    Insulin is most potent activator of lipogensis in adipose tissue. By binding its receptor, insulin facilitates the translocation of GLUT-4 and fatty acid transport proteins to the plasma membrane, thereby increasing the uptake of glucose and free fatty acids. Additionally, insulin activates lipogenic and glycolytic via peroxisome proliferator activated receptor γ (PPARγ; Kersten, 2001). PPARγ stimulates several lipogenic enzymes, including adipocyte binding proteins, LPL, fatty acid transport protein, ACS, and phosphoenol pyruvate carboxykinase (Kersten et al., 2000). Further, insulin stimulates the translation of element binding protein-1 (SREBP-1). SREBP-1 regulates the expression of PPARγ in adipose tissue and the hepatic lipogenic enzymes HMG-CoA reductase, LDL receptor, and fatty acid synthase (Horton & Shimomura, 1999).
    Compared with the pro-lipogenic effects of insulin, growth hormone inhibits lipogenesis in adipose tissue (Kersten, 2001). According to Etherton (2000), GH reduces specifically increase adipocyte insulin resistance without affecting whole body insulin sensitivity. As a result, GH decreases adipocyte acetyl-CoA carboxylase (ACC), fatty acid synthase, and glucose-6-phosphate dehydrogenase. GH also reduces lipogenesis by inactivating transcription factors Stat5a and Stat5b (Teglund et al., 1998), which stimulate lipogenesis via increased PPARγ expression (Wakao, Wakao, Oda, & Fujita, 2011).


    Lypolysis
    The catabolic process whereby TAG is broken down into a glycerol and three non esterfied fatty acids is referred to as lipolysis. In adipose tissue, intracellular TAG are acted upon by adipose triglyceride lipase (ATGL), hormone-sensitive lipase (HSL) and monoacylglycerol lipase (MGL; Lafontan & Langin, 2009). Regulation of lipolysis is achieved via the opposing actions of catecholamines and insulin modulating cAMP concentrations. In brief, catecholamines bind β-adreneric receptors (β-AR) coupled to G proteins, resulting in the generation of cAMP, activation of PKA, and phosphorlyation of HSL (Houston, 2006). In contrast, the interaction of insulin and the receptor activates the PI-3K/Akt pathway, resulting in the generation of phosphodiesterase-3B and hydrolysis of cAMP (Carmen & Victor, 2006). Other factors also positively and negatively affect lipolysis, such as glucocorticoids and prostaglandins, respectively (Lafontan & Langin, 2009). In particular, GH positively influences lipolysis (Samra et al., 1999). Although the exact mechanism has yet to be elucidated, Vijayakumar, Novosyadlyy, Wu, Yakar, and LeRoith (2010) suggested that GH increases HSL activity and translocation to the lipid droplet by augmenting β-AR cAMP generation.
    Fatty Acid Translocation
    Once fatty acids are taken up by skeletal muscles they must be activated and transferred across the two membranes of the mitochondria before participating in beta oxidation. Activation occurs on the outer mitochondrial membrane and involves the attachment of a coenzyme to the fatty acid via muscle ACS. Next, the fatty acyl-CoA is transported across the outer and inner mitochondrial membranes via the carnitine palmitoyl transferase (CPT) I and II complex, respectively (Brookes et al., 2005a). In addition to CPT, fatty acyl-CoA are also transported across the mitochondrial membrane via fatty acid translocase (FAT/CD36; Holloway, Bonen, & Spriet, 2009).
    Variances in mitochondrial fatty acid oxidation rates between individuals have been correlated with differences in the content of mitochondrial CPT and FAT/CD36 (Holloway, Luiken, Glatz, Spriet, & Bonen, 2008). Based on the involvement of intramuscular carnitine in fatty acid oxidation, supplement companies have advertised l-carnitine as an ergogenic aid that may improve body composition and exercise performance (Borum, 2000). Ingestion of l-carnitine, however, does not elevate intramuscular carnitine levels (Kraemer, Volek, & Dunn-Lewis, 2008), improve fat oxidation (Broad, Maughan, & Galloway, 2011), aerobic and anaerobic performance (Smith, Fry, Tschume, & Bloomer, 2008), or body composition (Wutzke & Lorenz, 2004). In contrast oral ingestion, carnitine infusion in humans (Stemphens et al., 2006) and increased expression of CPT in rats has been shown to increase fatty acid oxidation (Bruce et al., 2009). Therefore, methods that increase intramuscular carnitine concentrations may improve body composition by increasing mitochondrial fatty acid oxidation via enhanced translocation.
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