Page 534 - Small Animal Clinical Nutrition 5th Edition

552 Small Animal Clinical Nutrition

with diabetes mellitus usually improves or resolves as glycemic
Table 28-2. Key nutritional factors for hyperlipidemia. control is achieved.
VetBooks.ir Disorder Factor Dietary recommendations Diabetic dogs with excess serum triglyceride concentrations
Triglycerides Feed a food that reduces
Hyperlipidemia
serum triglycerides appear to be at risk for developing acute pancreatitis or
Restrict dietary fat (<12% dry pseudopancreatitis. Dietary fat restriction can be expected to
matter [DM]) lower the serum triglyceride concentration and may facilitate
glycemic regulation in dogs receiving insulin.
Feed a food that reduces
serum triglycerides and binds
cholesterol and bile acids PROTEIN-LOSING NEPHROPATHY
Increase dietary fiber: Hyperlipidemia, characterized by increased serum choles-
Dogs: ≥10% DM
Cats: ≥7% DM terol or triglyceride levels, may be detected in patients with pro-
teinuria due to glomerulonephritis or amyloidosis. An inverse
Add lipid-reducing drugs relationship between elevated blood lipids/lipoproteins and
(fibrates) if dietary manage-
ment alone is unsuccessful in decreased plasma albumin concentration has been reported to
controlling hyperlipidemia occur in patients with nephrotic syndrome. The actual patho-
genesis whereby the hyperlipidemia develops is complex and
appears to be due to a combination of factors involving
altered metabolism of lipoproteins (Bernard, 1982). Hyper-
Feline Inherited Hyperchylomicronemia cholesterolemia occurs inconsistently in dogs with heavy pro-
A primary, genetic disorder of young cats was found to alter teinuria.The lipoprotein profile of dogs and cats with nephrot-
chylomicron metabolism (Jones et al, 1983). Cats that had ic syndrome has not yet been characterized. The influence of
inherited this disorder developed a form of hyperlipidemia sim- hyperlipidemia on morbidity and mortality in nephrotic syn-
ilar to that reported to occur in miniature schnauzers. drome is unknown.

Secondary Disorders of Lipid Metabolism HYPERADRENOCORTICISM
Considering the prevalence of metabolic diseases that affect Hypercholesterolemia has been recognized in dogs with
lipid metabolism, it is possible that secondary hyperlipidemia hyperadrenocorticism (Cushing’s syndrome) without concomi-
affects more animals than primary hyperlipidemia. Several tant diabetes mellitus (Armstrong and Ford, 1989; DeBowes,
endocrine diseases, as well as renal and hepatic diseases, variably 1987; Barrie et al, 1993). Affected dogs have clear serum,
alter lipoprotein metabolism resulting in either hypertriglyc- increased plasma cholesterol and LDL-cholesterol levels, but no
eridemia or hypercholesterolemia. discrete clinical signs specifically attributable to excess choles-
terol. In a limited study of adult dogs confirmed to have hyper-
a
DIABETES MELLITUS adrenocorticism, only 30% were hypercholesterolemic. There
Hyperlipidemia secondary to diabetes mellitus in dogs and appears to be little diagnostic value to performing lipid determi-
cats may be characterized by hypertriglyceridemia and moder- nations in dogs suspected of having endogenous cortisol excess.
ate hypercholesterolemia (Ford, 1996; Armstrong and Ford, However, monitoring changes in a given patient’s cholesterol
1989; Barrie et al, 1993). In insulin-deficient states, clearance of profile may have prognostic value in dogs undergoing treatment.
chylomicrons is impaired due to insufficient activation of
lipoprotein lipase in vascular endothelial cells by insulin (Brown HYPOTHYROIDISM
and Goldstein, 1987). Examination of lipid profiles of diabetic Hypercholesterolemia is present in up to two-thirds of
dogs reveals lipemia, an increase in chylomicrons and VLDL hypothyroid dogs and is believed to result from impaired LDL
and a corresponding increase in triglyceride concentration. In clearance from the general circulation. It has been suggested
some diabetic dogs, excess serum cholesterol concentrations that an absolute triiodothyronine deficiency may lead to an
will be present independent of hypertriglyceridemia. In one increased hepatic cholesterol pool. In turn, LDL-receptor
study, diabetic dogs did not have cholesterol levels significantly activity is down regulated preventing excess sterol accumulation
different from those of a control population (Barrie et al, 1993). in the liver (Barrie et al, 1993). Atherosclerotic-type arterial
LDL-cholesterol, on the other hand, was increased presumably lesions have occasionally been reported (DeBowes, 1987). This
as a result of increased LDL synthesis.The clinical significance finding has led to the suggestion that cholesterol be included in
of this finding is unknown. an initial diagnostic screening for hypothyroidism. However,
Although a relationship between the quality of glucose regu- superior laboratory tests are available for evaluating thyroid dis-
lation and serum triglyceride levels has been recognized in peo- ease in cats and dogs and should be considered before serum
ple, it is unknown whether a similar relationship exists in dogs cholesterol evaluation.Therapy should be directed towards cor-
and cats. Lipemia retinalis in dogs and cutaneous xanthomato- recting the thyroid-hormone deficiency. Although hypothyroid
sis in cats are associated clinical findings that may be apparent people may experience decreased cholesterol levels after thy-
among insulin-dependent diabetics, particularly those with roid-replacement therapy is started, there is no apparent value
severe hypertriglyceridemia. The hyperlipidemia associated in monitoring cholesterol in affected dogs.