Increased platelet noradrenaline release in familial hypercholesterolaemia (FH)

273 AP@PROTEIN, LIPOPRBTEIN & RECEPTOR STUDIES IN NON-FAHILIAL HYPERCHOLESTEROLAEMIA HERITABLE HYPERCHDLESTEROLAEMIA

APOLIPOPROTEIN E PHEHOTYPE POLYMORPBISH & LIPOPROTEINS IN INSULIN TREATED DIABETES HELLITUS

Holliday M P, Winder A F & Wojciechowski

Winocour P H', Durrington P N 2, Tetlow L*, Ishola H 2, Hillier V 3 & Anderson O C'

A P.

Dept. Chemical Pathology, Royal Infflrmary & Medical School, Leicester. A panel of apoprotein and lipqorotein fraction detern/nations have been made in 46 individuals, both hypercholesterola~{dc and noIr~)chelesterola~dc, from 7 fan/lies defined as expressing polygenic hypercholesterola~ia on the basis of: (i) the absence of clinlcal features of Familial Hyoercholesterola~a (ii) the absence of a monogenic pattern of inheritance and (iii) normal expression of LEL receptors. No qualitative variants, associated with total cholesterol ware observed in the c
Oepts. o£ Mediclne ' z , Computation 3 & B i o c h e m i s t r y * , U n i v e r s i t y off Manchester. Apolipoprotein (Apo) E, a cc~psnent of chylcnieron remnants, VtEt ard PD_, tress an important role in receptor binding. ADO E occurs as } genetic isoforms (El, ES, E4). E2 hcn~zygeaity ard glucose intolerance occur in Type III hyperlipoproteina~ia (PLP), where atheroma distribution is similar to insulin treated diabetics (ID). Apa E phenotypes ~ere determined by isoelectric focussing and lipoproteins analysed in 7S IO. 7 (9%) ~ere homozygous for El, one having Type Ill ~kP. 7% ware EI/ES, 19% ES/ EZ¢ and 65% N~/ES. Cholesterol, L£t and Ppo B ~ere least in S_2 h~mszygotes and heterezygotes, hi,nest in E_3/E4 diabetics, and intermediate in E3 [mrozygotes. L£t cholesteroi/Aco B ratio was increased irrespective of Apo E prenotype. Groups ~ere of similar age, sex, body mass, insulin dose, glycaemdc eontrel, trigiyceride, bO_, REL2 s d H~L3 cholesterol (C). ResiOsal C peptide secretion was greater and dlat~£es ct~ation less in E2
INCREASED PLATELET NORADRENALINE RELEASE IN FAMILIAL HYPERCHOLESTEROLAEMIA (FH)

APOLIPOPROTEIN (APO) B BNA POLYMORPHISM ASSOCIATED WITH BIFFERENCE5 IN LDL ME[ABOLISH

Smith C C T, Wilson A P, Prichard B N C* & Betteridge O S. Cardiovascular Research Lob., DecCa. of Medicine & Clinical Pharmacology*, University College & Middlesex School of NL~dteine, L c ~ .

D ~ s t T H*, Houlston R 2, Caalake ~ , ~ries S ~ , RLmonries S E 2, Packazd O O ~ & 9 ~ n e r d S*. Dept. Biod-exEstry, Glasgc~ Royal InfiFnary* & %Jsiey Research Institute, Crazing Cross Hospital, Lc~on.2 .

have measured erds:jengLs noradrenaline release ficm washed platelets inckbated with ard without O . ~ t s / m l thrc~in in 14 noznals (28.2+1.5y; mean + ~ ) and 6 FH patients (28.5+3.@). Plat~et aggregatTon i r ~ by thrc~in was d~tezmined and sqsematant noradreealine concentrations assessed by RFtC. lhrcr~in indJced irreversible aggregation of washed platelets in both nozmal and FH subjects, tnder restlng conditions noradrenaline release was 15~/o greater (p
Restriction £ragnent lerNth Fxiymaz~Jis% (F#lPs) o£ tk~ g~-e codirq_ for aBolipoprotein B ~sre i<~