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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The contribution of dietary cholesterol to hypercholesterolemia in diabetic rats fed chow ad libitum was evaluated. Diabetes was induced with streptozotocin, and the intake, absorption, and subsequent tissue distribution of dietary cholesterol were measured. Absorption was measured as the difference between [3H]cholesterol intake and fecal 3H-labeled neutral sterol excretion, using both [14C]sitosterol (added to diet) and [14C]cholesterol (added to feces) as recovery markers. [3H]Cholesterol absorption was underestimated by 1-3% using [14C]sitosterol as a recovery standard, due to the 7-8% absorption of sitosterol. After 3 weeks of diabetes, rats were hyperphagic, thereby increasing dietary cholesterol intake 2-fold. [3H]Cholesterol absorption was significantly increased from 69% in controls to 78% in diabetics, whereas [14C]sitosterol absorption was unaffected. With increased dietary cholesterol intake and decreased whole body cholesterol synthesis (Diabetes. 1983. 32: 811-819), influx from diet equaled for exceeded influx from synthesis. The amounts of 3H-labeled neutral sterol recovered from the small intestine, periphery, and plasma were increased 3- to 4-fold in the diabetic rats. Furthermore, the degree of hypercholesterolemia in diabetic rats was directly related to the fraction of plasma cholesterol derived from the diet. We conclude that the 2.3-fold increase in absorbed dietary cholesterol resulting from hyperphagia and, to a lesser extent, from increased fractional absorption, contributes to the hypercholesterolemia of diabetic rats fed chow ad libitum.
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PMID:Evaluation of the contribution of dietary cholesterol to hypercholesterolemia in diabetic rats and of sitosterol as a recovery standard for cholesterol absorption. 403 27

Thirteen cats with diabetes mellitus were evaluated. Clinical signs included polydipsia, polyuria, polyphagia, lethargy, and weight loss. Results of physical examination included obesity, hepatomegaly, mild seborrhea sicca, muscle wasting, and dehydration. One cat walked plantigrade and was suspected of having a diabetic neuropathy. Persistent hyperglycemia, glucosuria, high liver enzyme activities, hypercholesterolemia, hyperproteinemia, and low electrolyte concentrations were the common laboratory findings. In 3 cats diabetes mellitus developed after megestrol acetate therapy; 2 of these cats required only temporary insulin treatment. In a 3rd cat, which had no history of receiving diabetogenic drug therapy, remission of diabetes mellitus also was observed. Serum insulin and plasma glucose concentrations were determined in 6 cats after administration of an intermediate-acting insulin (isophane insulin) and in 3 cats after administration of a long-acting insulin (protamine zinc insulin). The insulin concentration peaked 2 to 6 hours after the injection of intermediate-acting insulin and 6 to 12 hours after the injection of long-acting insulin. The lowest glucose concentration was recorded 4 to 8 hours after injection of intermediate-acting insulin, and 6 to 12 hours after injection of long-acting insulin. It was concluded that, although insulin therapy must be adjusted to the individual, the diabetic cat usually requires twice-daily administration of isophane insulin; however, the protamine zinc insulin can be given once daily for satisfactory control.
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PMID:Insulin therapy in cats with diabetes mellitus. 629 64

We examined the effect of streptozotocin-induced diabetes on the rate-limiting enzyme in cholesterol synthesis, 3-hydroxy-3-methylglutaryl CoA reductase (EC 1.1.1.34), in liver and small intestine of rats. During the acute phase of insulin deficiency (first day), food intake, plasma cholesterol, and reductase specific activity in liver all decreased. By 3 days, food intake, plasma cholesterol, and reductase activity in small intestine were all increasing. After 1 week, total reductase activity in small intestine was 2.5 times normal, whereas activity in liver remained low. Thus diabetes shifted the major site of cholesterol synthesis from the liver to the small intestine. These data support the proposal that hyperphagia by diabetic rats leads to increased input of both dietary and newly synthesized cholesterol by the small intestine into thoracic lymph and thereby contributes significantly to their hypercholesterolemia. The possibility that diabetes affected the F--inhibitable activation of reductase in vitro was also tested. There was no evidence of an effect in small intestine, but activation of reductase in vitro was decreased by 1/3 in liver. These data suggest that, in liver, either the activity of the activator was decreased or the fraction of reductase in the active state was increased after more than 12 hr of insulin deficiency.
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PMID:Total hydroxymethylglutaryl CoA reductase activity in the small intestine and liver of insulin-deficient rats. 704 79

The present study was undertaken to study the effects of chronic treatment with lisinopril on the cardiovascular complications in streptozotocin (STZ) diabetic and deoxycorticosteroneacetate (DOCA) hypertensive rats. Injection of STZ produced severe glycosuria (> 2%), hyperglycemia, hypoinsulnaemia, polydypsia, polyphagia and loss of body weight. It also produced hypothyroidism, hypercholesterolaemia, hypertriglyceridaemia, hypertension, bradycardia and decreased left ventricular developed pressure (LVDP). Elevation in serum creatinine level and increased activity of liver enzymes were also found in STZ treated animals. DOCA by itself did not produce any change in blood glucose but reduced serum insulin levels in non-diabetic animals. However, in the diabetic group, DOCA reduced blood sugar levels. Treatment of STZ-diabetic rats with DOCA did not aggravate cardiac depression or hyperglycaemia. Treatment of rats with lisinopril (1 mg kg-1, p.o. daily for six weeks), in diabetic and diabetic hypertensive animals prevented STZ induced loss of body weight and hypertension, bradycardia and hypothyroidism. It also prevented STZ induced hyperglycemia and hypoinsulinaemia in both diabetic and diabetic hypertensive animals. There was a reduction in cholesterol, triglyceride, and LDL levels; the ratio between total cholesterol to HDL and LDL to HDL and an improvement in LVDP at higher filling pressure in diabetic as well as diabetic hypertensive animals. Treatment with lisinopril also prevented hypertrophy and elevated levels of serum creatinine, SGOT and SGPT in diabetic animals. In conclusion, the present data suggests that STZ-DOCA model may not be considered as the ideal model for the study of cardiovascular complications of combined treatment hypertension and diabetes. However, the present investigation presents a number of beneficial effects of lisinopril treatment in diabetic with or without hypertensive rats and it may be considered as one of the drugs of choice in treatment of hypertension when it is associated with diabetes mellitus.
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PMID:Effects of chronic treatment with lisinopril on cardiovascular complications in streptozotocin diabetic and DOCA hypertensive rats. 907 44

Calcium antagonists have been reported to alter insulin secretion and insulin sensitivity. However, there still exists a controversy over the benefits of calcium antagonists in the conditions when diabetes mellitus and hypertension coexist. In the present study the effects of six-week chronic amlodipine treatment (5 mg kg-1 p.o.) on insulin sensitivity and serum lipid levels in streptozotocin (STZ)-diabetic and spontaneously hypertensive (SH) rats were investigated. Intravenous injection of STZ produced glucosuria (> 2%). hyperglycaemia, hypoinsulinemia, polydipsia, polyphagia, loss of body weight, hypercholesterolemia, hypertriglyceridaemia, hypertension and bradycardia. SH rats were found to have significantly higher insulin levels compared to their Wistar controls. Treatment of rats with amlodipine in diabetic and diabetic-hypertensive animals significantly prevented STZ-induced loss of body weight, hypertension and bradycardia. It also significantly prevented STZ-induced hyperglycaemia in both STZ-diabetic Wistar and SH rats. The insulin levels were decreased in the non-diabetic treated Wistar rats but were unaltered in the non-diabetic SH and the diabetic Wistar and SH rats. There was a significant reduction in cholesterol levels in diabetic Wistar and SH rats. In conclusion the present study revealed beneficial effects of amlodipine treatment in hyperinsulinemic, diabetic and/or hypertensive rats.
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PMID:Effects of chronic treatment with amlodipine in streptozotocin-diabetic and spontaneously hypertensive rats. 929 5

An unusual combination of three endocrinopathies found in one dog is described. A six-year-old, spayed female, mixed-breed dog presented with polyuria, polydipsia, polyphagia, and weight loss. She was diagnosed with diabetes mellitus but was suspected of having insulin resistance and was diagnosed subsequently with hyperadrenocorticism. Persistent hypercholesterolemia led to the suspicion and eventual diagnosis of hypothyroidism. The dog has responded well to medical therapy, and her clinical signs and biochemical changes have resolved. A literature search did not identify a similar-reported polyendocrinopathy.
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PMID:Diabetes mellitus, hyperadrenocorticism, and hypothyroidism in a dog. 959 Apr 47

The industrialized world is confronted to a real epidemic of metabolic diseases triggered by overeating and sedentarity. Obesity, hypercholesterolaemia, diabetes mellitus and the metabolic syndrome associated to insulin resistance are well-known cardiovascular risk factors which all contribute to increase both morbidity and mortality, to alter the quality of life and to markedly increase the budget of the social security. Preventive measures should be taken urgently in order to correct such a dangerous trend for the public health.
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PMID:[The epidemic of metabolic diseases, a major problem of public health]. 1022 Oct 60

The proponents of fat-restricted diets for children argue that low-fat diets given in childhood will prevent the development of atherosclerosis in adulthood, low-fat diets given a childhood will condition children to prefer low-fat diets in adulthood, and low-fat diets for children are safe. There is no evidence that low-fat diets in childhood will prevent atherosclerosis in adulthood. In fact, studies of migrating populations indicate that immigrants to the United States from Third World countries who consumed low-fat diets in childhood take on the character of their new environments, including higher serum cholesterol levels and more coronary disease. The prevalence of fatty streaks in childhood bears little relationship to the prevalence of atheromatous plaques in adulthood. In fact, girls have more aortic fatty streaks and higher serum cholesterol values in childhood than boys, but fewer plaques in adulthood and less coronary disease. From the PDAY study, it has also been learned that hypercholesterolemia in childhood enhances fatty streak formation, but not that of plaques. It now seems established from autopsy studies that the progression of atherosclerosis from fatty streaks to plaque is arrested in childhood and does not begin to a significant extent until after puberty in males and after menopause in females. So the oft-repeated statement that atherosclerosis begins in childhood is semantically true but very misleading. The particularly harmful form of atherosclerosis (the plaque) does not become significant until much beyond puberty. The effects of low-fat, low-cholesterol diets on serum lipids and lipoproteins are of a lesser magnitude in children than in adults. The 0.78 mmol/L decrease in LDL cholesterol in the intervention group from controls (change 1.5%) in the DISC study was biologically insignificant and reflects the tighter control of lipoprotein and cholesterol synthesis in children compared with adults. It must be remembered that the human body synthesizes all of the cholesterol it needs from acetyl CoA. In general, the larger the amount of dietary cholesterol absorbed, the smaller the rate of biosynthesis of cholesterol. In some adults and most children this homeostatic control is nearly perfect, but in many adults the correction in biosynthesis of cholesterol with increased dietary input is imperfect and LDL cholesterol values increase. The second argument of the proponents of low-fat diets for children is that they are conditioned to continue low-fat diets in adulthood. From the studies of Birch and Fisher (51) this prediction seems unlikely. These investigators found that restricting access to palatable foods enhanced the interest of 3- to 5-year-old children in those foods and increased their desire to obtain and consume those foods. They concluded that "stringent parental controls can potentiate preference for high-fat energy-dense foods, limit children's acceptance of a variety of foods and disrupt children's regulation of energy intake." Brosin (52) has also observed that food restriction in childhood may lead to gluttony in adulthood. Finally, the claim that low-fat diets are safe in childhood is based on observations over too short a time to establish safety. It is true that growth and development of children studied in the DISC study was not changed from the expected increments, but that is not proof of long-term safety. In addition, the lower content of essential nutrients in low-fat, low-cholesterol diets (calcium, zinc, magnesium, phosphorus, vitamin E, vitamin B-12, thiamin, niacin, and riboflavin) must be considered along-term risk (53,54). Furthermore, the published studies of the safety of low-fat diets have been conducted under intensive surveillance in medical centers, conditions very different from those in the homes of free-living families.
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PMID:Is it wise to restrict fat in the diets of children? 1064 98

India is amidst a demographic transition showing an ageing trend. This will increase non-communicable diseases including diabetes which is already showing an increasing trend. With scanty literature existing on elderly diabetics (> 60 years of age), it was decided to study the clinico-laboratory and complication profile of this group of patients. Fifty consecutive elderly diabetics were studied and evaluated for ECG, chest x-ray, blood sugar, urea, creatinine, lipid profile, proteinuria, motor nerve conduction velocity and autonomic neuropathy. Duration of diabetes varied from one month to 28 years. Fifty-six per cent of the patients presented with classical symptoms of polyuria, polyphagia and polydipsia. Hypertension was present in 40% and cataract in 54% of the patients. Eighteen per cent were obese, 52% had evidence of peripheral neuropathy while 56% had autonomic neuropathy. Background diabetic retinopathy was present in 56%, pre-proliferative retinopathy and maculopathy in 4% each; hypertensive retinopathy in 10% of patients; 44% had microproteinuria and 8% had chronic renal failure. Hypercholesterolaemia was present in 64% and hypertriglyceridaemia in 42% of the patients with 26% having coronary artery disease. Sixty per cent were harbouring infections--20% had foot infections, 14% had tuberculosis and 10% had urinary tract infections. Ninety-two per cent of the patients were aware of their disease but 62% were not aware of the complications and of the need for strict dietary and drug compliance. There was a high prevalence of associated diseases viz, osteoarthritis, cataract, hypertension, hepatitis and parkinsonism. Therefore, this study brings out the need to have a holistic and multidisciplinary approach for management of elderly diabetics who constitute a heterogeneous group with distinct health care problems.
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PMID:Clinical and laboratory profile of diabetes in elderly. 1065 95

Aromatase, the enzyme responsible for the conversion of androgens to estrogens, is present in the mouse gonads, brain, adipose tissue and bone. Depletion of endogenous estrogens in the aromatase deficient mouse (ArKO) caused by the targeted disruption of the Cyp19 gene resulted in an impairment of sexual behaviour and an age-dependent disruption of spermatogenesis. This disruption occurred during early spermiogenesis, due possibly to increased number of apoptotic round spermatids. Development of obesity was associated with ageing, decrease in lean mass, hypercholesterolemia, hyperleptinemia, and insulin resistance and hepatic steatosis. However, it was not correlated with hyperphagia but to decreased physically-active behaviour. ArKO mice also developed osteoporosis. Thus, studies using the ArKO mice model has led to several insights into the multiple roles played by estrogens in the development and maintenance of fertility, sexual behaviour, lipid metabolism and bone remodelling.
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PMID:Effect of estrogen deficiency in the male: the ArKO mouse model. 1216 Sep 96


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