106
HDL2 to HDL3 and enzyme lipoprotein lipase (LPL) breaks down the triglycerides
to free cholesterol which is then taken up by HDL to liver. Free cholesterol is esterified to cholesteryl ester by lecithin cholesterol acyltransferase (LCAT). Cholesteryl
ester transfer proteins (CETP) transport cholesteryl ester from HDL2 to triglycerides, VLDL and LDL [22]. The thyroid hormones influence the lipid metabolism in
various ways. Thyroid hormones regulate cholesterol biosynthesis by influencing
β-Hydroxy β-methylglutaryl-CoA (HMG-CoA) reductase. The T3 hormones control the LDL receptors gene activation process by binding to thyroid hormone
response elements (TRE’s) and also by controlling SREBP-2. Moreover, T3 upregulates LDL receptors by protecting the oxidation of LDL. Thyroid hormones can
also influence the lipoprotein metabolism and reverse transport of cholesterol by
increasing the activity of certain enzymes such as CETP, LCAT, LPL, hepatic
lipases. The T3 is also known to up-regulate the expression of apo lipoprotein
(ApoAV), which regulates serum triglycerides levels (Fig. 6.4) [22].
Hypothyroidism and Dyslipidaemia
Overt hypothyroidism is accompanied by increased total cholesterol and LDL concentration owing to decreased activity of HMG-CoA reductase. This is due to
impact of thyroid hormones on SREBP-2. Moreover, a decrease in catabolism of
LDL, decreased activity of LPL and ultimate decrease in clearance of triglycerides
rich lipoproteins are associated with overt hypothyroidism. Studies have also shown
that hypothyroid individuals may also develop type III hyperlipoproteinemia
because of increased levels of cholesterol and apo lipoproteins E, rich particles of
VLDL and intermediate density lipoprotein (IDL). Elevations in the plasma level of
HDL cholesterol can also be seen in hypothyroid individuals. This occurs as a result
of decreased activity of CETP and an ultimate decreased conversion of HDL2 to
VLDL [22, 23].
In subclinical hypothyroidism dyslipidaemia, patients are usually observed with
increased total cholesterol, LDL cholesterol, increased triglycerides and decreased
HDL cholesterol. Increased level of anti-thyroid antibodies, despite normal TSH
levels, may also cause a rise in plasma cholesterol levels (Fig. 6.5) [22, 23].
Hyperthyroidism and Dyslipidaemia
In hyperthyroid patients, plasma levels of cholesterol decrease due to increased
activity of catabolic pathways leading to enhanced synthesis and degradation of
lipids. These hypolipidemic effects can be attributed to high cellular uptake and
excretion of cholesterol in bile salts. Increased levels of thyroid hormones cause the
accelerated lipogenesis in liver, which may lead to hypertriglyceridemia in hyperthyroid patients. Furthermore, serum LDL, HDL and subfraction HDL2 found to be
Y. H. Khan et al.
HDL2 to HDL3 and enzyme lipoprotein lipase (LPL) breaks down the triglycerides
to free cholesterol which is then taken up by HDL to liver. Free cholesterol is esterified to cholesteryl ester by lecithin cholesterol acyltransferase (LCAT). Cholesteryl
ester transfer proteins (CETP) transport cholesteryl ester from HDL2 to triglycerides, VLDL and LDL [22]. The thyroid hormones influence the lipid metabolism in
various ways. Thyroid hormones regulate cholesterol biosynthesis by influencing
β-Hydroxy β-methylglutaryl-CoA (HMG-CoA) reductase. The T3 hormones control the LDL receptors gene activation process by binding to thyroid hormone
response elements (TRE’s) and also by controlling SREBP-2. Moreover, T3 upregulates LDL receptors by protecting the oxidation of LDL. Thyroid hormones can
also influence the lipoprotein metabolism and reverse transport of cholesterol by
increasing the activity of certain enzymes such as CETP, LCAT, LPL, hepatic
lipases. The T3 is also known to up-regulate the expression of apo lipoprotein
(ApoAV), which regulates serum triglycerides levels (Fig. 6.4) [22].
Hypothyroidism and Dyslipidaemia
Overt hypothyroidism is accompanied by increased total cholesterol and LDL concentration owing to decreased activity of HMG-CoA reductase. This is due to
impact of thyroid hormones on SREBP-2. Moreover, a decrease in catabolism of
LDL, decreased activity of LPL and ultimate decrease in clearance of triglycerides
rich lipoproteins are associated with overt hypothyroidism. Studies have also shown
that hypothyroid individuals may also develop type III hyperlipoproteinemia
because of increased levels of cholesterol and apo lipoproteins E, rich particles of
VLDL and intermediate density lipoprotein (IDL). Elevations in the plasma level of
HDL cholesterol can also be seen in hypothyroid individuals. This occurs as a result
of decreased activity of CETP and an ultimate decreased conversion of HDL2 to
VLDL [22, 23].
In subclinical hypothyroidism dyslipidaemia, patients are usually observed with
increased total cholesterol, LDL cholesterol, increased triglycerides and decreased
HDL cholesterol. Increased level of anti-thyroid antibodies, despite normal TSH
levels, may also cause a rise in plasma cholesterol levels (Fig. 6.5) [22, 23].
Hyperthyroidism and Dyslipidaemia
In hyperthyroid patients, plasma levels of cholesterol decrease due to increased
activity of catabolic pathways leading to enhanced synthesis and degradation of
lipids. These hypolipidemic effects can be attributed to high cellular uptake and
excretion of cholesterol in bile salts. Increased levels of thyroid hormones cause the
accelerated lipogenesis in liver, which may lead to hypertriglyceridemia in hyperthyroid patients. Furthermore, serum LDL, HDL and subfraction HDL2 found to be
Y. H. Khan et al.