L-37___38 - R GU 0F LIPI ' B IS Metabolic regulation is...

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Unformatted text preview: R GU 0F LIPI ' B IS Metabolic regulation is achieved by enz es . metabolic regulation by allosteric control . integrative aspects of regulation 1, o o o I c 11 co Binding of the glilggggn to the plasma membrane results in the subsequent phosphorylation of enzymes by protein kinases. ' a. acetyl CoA carboxylase (inhibited) b. hormone sensitive lipase (activated) c. pyruvate dehydrogenase (inhibited) With the following results: a. decreased fatty acid synthesis b. increased gluconeogenesia c. increased mobilization of stored fats 11. MW 1, Palmitoyl CoA inhibits fatty Acid synthesis by allosteric inhibition of acetyl CoA carboxylsse - 2. decreased fructose 2.6 diphosphate which decreases phosphofructokimue» III. 0 CO 0 I 1. Binding of IRSULIN to the plasma membrane results in the Subsequent dephosphorylation of the following enzymes by phosphoprotein phosphatase . a. acetyl CoA carboxylase (activated) b. hormone sensitive lipase (inactivated) —-— c. pyruvate dehydrogenase (activated) With the following results: a. increased fatty acid synthesis b. decreased gluconeogenesis c. decreased mobilization of stored fatty acids 2. Changes of enzyme synthesis a. fatty acid synthesis induced b. acetyl, Co A carboxylase induced c. adipose lipoprotein lipase induced mom a. acetyl CoA carboxylase is activated by citrate b. carnitine palnitoyl transferase is inhibited by malonyl CoA c. increases F 2.6 bisphosphate which increases PFK-l and decreases Fructose l . 6-bisphosphatase I37 glycerol Triacyl glycerols Stefoids + Phospholipids Cholesterol Ketone Glucose Bodies ‘ ATP 2 CO: ’3 8 (DE LETEP) 139 Phospholipids 1. Membrane constituents . precursors of triglycerides . storage of poly uns precursors) 2 3. precursors of secon 4 5. lung surfactants 140 b. 0. P05 01 dadTrlcereloste1 mgogk1 foofifi, % a H o. I o" h a“; «1‘60’? "4 - (guy A 'rlxosf‘whdsat CLOlIhC, "‘h‘1£32‘7“r°‘ (T6) Fatty acids are deriv ad from the fatty acid bioaynthetic pathway. The head group is transferred to y two mechanisms depending on the phospholipid to. he made. OER c:£f’ we» 0 ®®41+fdka '?L. cmP 0E X0” (at: 'P) 141 e. Triglycerides are made from diacylglycerol. f. Regulation- The cytidylyl transferase (CT) which catalyzes the formation of CDPcholine from CTP and phosphorylcholine is the rate limiting enzyme in PL biosynthesis. ’ ('9 cu en Erin ‘ 9’ M5 0 ‘0 z. 2. d” 3 + C'I‘P ----> cviidcubaixo-gm CHLCl-L- [ll-CH3 ’ 363 e _b _ ~ a,ch Phosphoryloholine GDP choline + PPi. 142 _—-—-—" cu,-ou l-lO-l -H glycerol 3- phosphate euro-£4)- fatty acyl CoA 0 ' euro-E R, dwlme. I fill, HO-CH I Ho-ca,cn,.N-cn, cu,~o- - l G - CH: . fatty acyl CoA ATP . CH , | J on o—g R. ‘ -0'g'003rCHr’ngs l C CD P at“. ... _ 11,- out _ cm _ H, R. CH. l 4% I Eat “"° CH;o- o. R, can C1? _ I add CH,-O-§»O‘§-cyudmo H10 _ - CH, | inositol Cy CHI-CH3 'N'CH’ _ _ Ana) . (Inn—03R. H MM, 3 did c: ¢chlw|iue “3'0?” 1," H V l CH,- 0-H fin-0g R, fatty m—lio-cn acyl CoA l . ' CH,-O- ~O-inositol secondary mossengm phosphatidyl ‘cholino (lecithin) tegulate cellular metabolism Triacylglycerol (TO) I43 Cholesterol Qiosygthesis a b c d e 3c: ——->CB --"'> CG-—-> C3'“"-> Cm "'"-> C15"'“'> C30 "--> 01101 I HHGCOA MVA a. HMGCoA synthase is common to sterol and ketone body synthesis. b. HMGCoA reductase makes mevalonate (MVA), the key and first intermediate of sterol biosynthesis. This is a highly regulated step. ‘c. An active isoprene is made which may combine with d. Two Cu units dimerize to form squalene a 0“ molecule. e. Squalene is cyclized using 0, and many enzymes to give cholesterol. - f. The whole process is very energy-dependent in terms of ATP and NADPH . b. steroid hormones such as - progesterone (steroid precursor of other steroids and regulator of events during pregnancy) ~ cortisol (glucocorticoid promotes gluconeogenesis and is anti-inflammatory agent) - aldosterone (mineralocorticoid, regulates ion balance in kidney) - estrone (female sex hormone, supports female characteristics) - testosterone (male sex hormone, promotes male sexual development and maintains male sex characteristics) 144 0 ” "-‘HL—OH Cl 5 Co” C“; (in) 2 NADPH Cl:- cH + CoASH 140-3;ch Ha~ I” 3 3 acetyl CoA —)_.9 CH; —‘\fi (i L ('0 " 2 NADP‘ coa HMG 30A HMG C A mevalonato (1mm) 0 . ‘ reductase f3 ATP >=\ 5 . C . - CIOFP .\ O 0 H017? c 3 {Ojg-O-g-o- flimsy! pyrophosphate (Cu) ' .. - isopentenyl pyrophosphato (C, PP) "\ 0} \ \ squaleno (0,.) cholesterol (C1,) Vi! D, . i V ‘ 11% ' ’ who PM \ I l °‘ / O /‘ progesterone (0,.) NADPH +0; 9W (:0 --0H Testosterorie (Cw) Aldosterone cortisol H I 145 estrous m (C '8) a. C. d. f. o ote' 5 These are high molecular weight complexes of specific proteins and lipids which function to transport lipids in the blood. These include very low density (VLDL) , low density” (1.01.), intermediate density. (IDL) and high density (Hop) lipoprote ins . . Very low density lipoprotein, VLDL, and chylomicrons are the richest in lipid and lowest in protein. They function primarily to deliver lipid to tissues. High density lipoproteins, , ( enriched in protein relative to lipid). Their primary function is to remove .cholesterol from t cholesterol. LDL and is picked up by peripheral tissue which is the mechanism by which cholesterol- is delivsred to peripheral tissues. 146 Wc\a\>0\{sm thopm‘ciu 147 Re lation of Cholesterol Bios thesi Synthesis of LDL receptors decreases with increased cholesterol Synthesis of HMG CoA reductase decreases with increased cholesterol 148 S ...
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L-37___38 - R GU 0F LIPI ' B IS Metabolic regulation is...

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