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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hyperlipaemia is an important condition in ponies, not just because of the seriousness of the clinical signs and biochemical changes involved, but because of the distress it causes owners and breeders that have had animals suffer from it. Hyperlipaemia occurs most commonly in fat ponies in late pregnancy and is rarely seen in larger horses. The syndrome has similarities with conditions in other species but the definitive aetiologies are not yet known. The condition in ponies is undoubtedly related to stress. The biochemical mechanisms involved in equine hyperlipaemia are considered and an hypothesis of possible pathogenesis is put forward. This hypothesis is tested by presenting the results of a preliminary study to evaluate glucose and lipid metabolism in horses and ponies. It appears that the pony is markedly insensitive to insulin compared to larger horses which means that triglycerides are more readily mobilised and the animal is therefore susceptible to hyperlipaemia in a situation of negative energy balance. The effect of stress is to increase cortisol levels which only exacerbates the insulin insensitivity and so creates a vicious circle. The importance of an innate insulin insensitivity may also be important in the pathogenesis of such conditions as laminitis.
Vet Rec 1985 Apr 27
PMID:Current concepts of hyperlipaemia in horses and ponies. 389 Mar 49

According to recent knowledge, apolipoprotein E (apo E) plays a significant role in the homeostasis of intracellular cholesterol level in various tissues. Apo E deficient mice develop hyperlipidemia, and suffer from atherosclerosis in extracerebral blood vessels and neurodegeneration in the central nervous system. Furthermore, Walker et al. (Am. J. Path., 1997;151:1371-1377) demonstrated cerebral xanthomas of various sizes in the brain of apo E deficient mice. In the present study, it is illustrated that in the homozygous apo E deficient mice of advancing age, a great number of foamy macrophages extravasate from microvessels in thalamus and fimbria hippocampi, and scatter in the perivascular regions and migrate toward the ependyma, fimbria hippocampi, hippocampus, and thalamus. Here, it must be pointed out that under hyperlipidemia, although foamy macrophages made clusters in the perivascular region, the cerebral microvessels did not develop atherosclerosis. On the other hand, in the other cerebral regions such as cerebral cortex, caudoputamen, globus pallidus, and substantia nigra, macrophages did not appear and microvessels retained normal shapes, but the fluorescent granular perithelial (in short, FGP) cells accompanied by these vessels contained a certain amount of lipids. That is, in the cerebral cortex and caudoputamen, lipid components are detected in FGP cells and microglia, while in the globus pallidus and substantia nigra, they are mainly localized in astrocytes. The reason why the astrocytes in such defined regions contain, specifically, a high quantity of lipid components remains unsettled. Axonal degenerations are often represented in thalamus, globus pallidus, and substantia nigra. On the other hand, in the specimens of Wild-type mice, lipid components were observed only in FGP cells, and the vascular architecture took a normal profile. Any lipid laden macrophages and the axonal degenerations could not be detected through the cerebral parenchyma. Furthermore, it is also a noticeable finding that immunohistochemically, the FGP cells express a positive reaction against the antibody of apo E in the Wild-type mice, but those of homozygous apo E deficient mice are immunonegative. FGP cells are not only provided with the scavenger receptor, but also contribute to the lipid metabolism in the brain.
Anat Rec 1999 10 01
PMID:Regional difference of lipid distribution in brain of apolipoprotein E deficient mice. 1048 14

The influence of various pathological conditions on fructosamine levels in normoglycaemic dogs and cats was investigated. The most frequent and most pronounced deviations were found in animals with hypoproteinaemia, in which fructosamine was significantly lower than in the controls. In 66 per cent of the dogs and 67 per cent of the cats with hypoproteinaemia the levels were below the reference range. In the dogs the concentration of fructosamine was correlated with the level of albumin, but in the cats it was correlated with the level of total protein. Dogs with hyperlipidaemia and azotaemia also had significantly lower levels of fructosamine; 38 per cent of those with hyperlipidaemia and 47 per cent of those with azotaemia had fructosamine levels outside the reference range. No significant changes in fructosamine were detected in dogs or cats with hyperproteinaemia or hyperbilirubinaemia, or in cats with hyperlipidaemia or azotaemia.
Vet Rec 2001 Mar 24
PMID:Evaluation of fructosamine in dogs and cats with hypo- or hyperproteinaemia, azotaemia, hyperlipidaemia and hyperbilirubinaemia. 1132 52

Morphological changes in the hepatic sinusoid with old age are increasingly recognized. These include thickening and defenestration of the liver sinusoidal endothelial cell, sporadic deposition of collagen and basal lamina in the extracellular space of Disse, and increased numbers of fat engorged, nonactivated stellate cells. In addition, there is endothelial up-regulation of von Willebrand factor and ICAM-1 with reduced expression of caveolin-1. These changes have been termed age-related pseudocapillarization. The effects of old age on Kupffer cells are inconsistent, but impaired responsiveness is likely. There are functional implications of these aging changes in the hepatic sinusoid. There is reduced sinusoidal perfusion, which will impair the hepatic clearance of highly extracted substrates. Blood clearance of a variety of waste macromolecules takes place in liver sinusoidal endothelial cells (LSECs). Previous studies indicated either that aging had no effect, or reduced the endocytic capacity of LSECs. However, a recent study in mice showed reduced endocytosis in pericentral regions of the liver lobules. Reduced endocytosis may increase systemic exposure to potential harmful waste macromolecules such as advanced glycation end products Loss of fenestrations leads to impaired transfer of lipoproteins from blood to hepatocytes. This provides a mechanism for impaired chylomicron remnant clearance and postprandial hyperlipidemia associated with old age. Given the extensive range of substrates metabolized by the liver, age-related changes in the hepatic sinusoid and microcirculation have important systemic implications for aging and age-related diseases.
Anat Rec (Hoboken) 2008 Jun
PMID:Old age and the hepatic sinusoid. 1848 14

The rat Pck gene is orthologous to the human PKHD1 gene responsible for autosomal recessive polycystic kidney disease (ARPKD). Both renal and hepatic fibrocystic pathology occur in ARPKD. Affected humans have a variable rate of progression, from morbidly affected infants to those surviving into adulthood. This study evaluated the PCK rat, a model of slowly progressive ARPKD. This model originated in Japan and was rederived to be offered commercially by Charles River Laboratories (Wilmington, MA). Previous studies have described the basic aspects of PCK pathology from privately held colonies. This study provides a comprehensive characterization of rats from those commercially available. Rats were bred, maintained on a 12:12 hr light/dark cycle, fed (7002 Teklad), and water provided ad libitum. Male and female rats were evaluated from 4 through 35 weeks of age with histology and serum chemistry. As the hepatorenal fibrocystic disease progressed beyond 18 weeks, the renal pathology (kidney weight, total cyst volume) and renal dysfunction (BUN and serum creatinine) tended to be more severe in males, whereas liver pathology (liver weight as % of body weight and hepatic fibrocystic volume) tended to be more severe in females. Hyperlipidemia was evident in both genders after 18 weeks. Bile secretion was increased in PCK rats compared with age-matched Sprague Dawley rats. The PCK is an increasingly used orthologous rodent model of human ARPKD. This characterization study of hepatorenal fibrocystic pathology in PCK rats should help researchers select stages of pathology to study and/or monitor disease progression during their longitudinal studies.
Anat Rec (Hoboken) 2010 Aug
PMID:Disease stage characterization of hepatorenal fibrocystic pathology in the PCK rat model of ARPKD. 2066 6