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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lipid and carbohydrate metabolism abnormalities are reviewed with particular emphasis on the role of insulin and interrelationships between carbohydrate and lipid metabolism. The pathogenesis of atherosclerosis is discussed in terms of the association of abnormal circulating insulin levels. Some of the conditions associated with abnormal insulin levels and atherosclerosis are diabetes mellitis, hypertriglyceridemia, obesity, uremia, and oral contraceptive use. There is evidence that a proportion of subjects who have atherosclerosis or at risk have elevated circulating insulin levels. There is also increasing evidence that the arterial wall is an insulin-sensitive tissue. More women with myocardial infarction take oral contraceptives than controls do. Those who take the pill have 9 times the risk of others to develop cerebral ischemia or thrombosis. Many oral contraceptives cause abnormalities in glucose tolerance associated with elevated plasma insulin levels, and a degree of insulin resistance is induced. A number of the metabolic consequences of the pill may be caused by the elevated insulin levels.
Atherosclerosis 1977 May
PMID:The relationship of abnormal circulating insulin levels to atherosclerosis. 85 12

The authors analysed clinically 108 patients (61 males and 47 females), aged below 50 years treated at the department of neurology, because of acute cerebral ischaemia. Attention is called to risk factors such as arterial hypertension, heart disease, atherosclerosis, obesity and diabetes which may be the cause of earlier development of ischaemic changes in the central nervous system. In the analysed group in 18 cases cerebral thrombosis, in 23 cases embolism, in 31 cerebral circulatory failure were diagnosed. In 36 cases the cause could not have been established.
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PMID:[Acute cerebral ischemic disease in patients under the age of 50]. 88 1

The smooth muscle cell plays an important role in the process of atherogenesis, proliferating in the arterial intima and becoming filled with lipid during the course of the disease. In these experiments the effect of insulin and glucose on sterol synthesis in cultured rat arterial smooth muscle cells was studied. Arterial smooth muscle cells were cultured from pieces of intima and inner media of young rat aortas. The cells were grown in Petri dishes in culture medium with foetal calf serum and when confluent were exposed to insulin or glucose for 24 hours. Insulin in concentrations of 10 micromicron-100 millimicron per ml stimulated the incorporation of sodium [2-(14)C]acetate into non-saponifiable lipids and digitonin precipitable sterols. However, insulin had no effect on the incorporation of labelled mevalonate into cell sterols. Increasing concentrations of glucose in the medium up to 140 mM had had no effect on the incorporation of isotope into sterols, but higher concentrations of glucose caused cell damage and sterol synthesis was markedly depressed. These results may have relevance to the development of atherosclerosis in diabetes and obesity.
Atherosclerosis 1977 Jul
PMID:The effect of insulin and glucose on sterol synthesis in cultured rat arterial smooth muscle cells. 90 24

A long account of the many factors responsible form atherosclerosis (dysmetabolism, physical, genetic and familial factors, immunobiological features, diet) is followed by an assessment of obesity as a main risk factor in the local pathology of atherosclerosis. Results obtained in the treatment of obesity with chorionic gonadotropin and a 500 calorie standard diet are presented. These were highly satisfactory with respect to weight loss, tolerance, and marked improvement (or even normalisation) of blood lipid values, which were initially pathological in many cases.
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PMID:[Treatment of obesity with chorionic gonadotropins. Relations between obesity, dyslipidemia and arthero-arteriosclerosis]. 95 Oct 38

There appears to be a need to protect our young from an atherogenic way of life. The average male child today has one chance in three of a cardiovascular catastrophe before age 60. Atherosclerosis and the conditions which predispose appear to have their onset in childhood. Correctable precursors of cardiovascular disease have been identified, and their contribution to risk has been estimated not only for adults but for college students as well. An analysis of the combined impact of atherogenic risk factors indicates that they exert greater force early in life than later. Although the optimal time to begin prophylaxis is not established, there is evidence to suggest that measures instituted late in life when lesions are advanced is of only limited value. Prevention of atherosclerosis is best viewed as a family affair since the propensity to disease and contributing factors tend to be shared by family members. It is also difficult to implement effectively preventive measures which include dietary changes, weight control, exercise and restriction of cigarettes for one family member without involving the rest of the family. Optimal levels of the correctable precursors of cardiovascular disease are not established for children. However, the rise in serum lipids, blood pressure, weight and blood sugar observed in transition from childhood to adult life is not inevitable, or desirable. Paediatricians can alter the appalling cardiovascular mortality statistics by not allowing the process or the habits and conditions which promote it to reach an irreversible stage. Cardiovascular disease may well begin in childhood with "medical trivia" such as a tendency to obesity, moderate cholesterol and blood pressure elevations, lack of exercise and the cigarette habit. In some respects a heart attack at age 45 can be regarded as a failure of the paediatrician. Awaiting proof of the efficacy of the indicated prophylactic measures is not acceptable since this will be a long time in coming. We must learn how to correct risk factors effectively in childhood as soon as they appear. We must establish goals based on optimal as distinct from usual levels of risk factors. Paediatricians' resolve about prevention of atherosclerosis in childhood needs to be strengthened and we must develop a sense of urgency about this.
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PMID:Prospects for prevention of atherosclerosis in the young. 107 69

In a large autopsy series the relation between various measures of body build and aortic and coronary atherosclerosis, coronary stenosis, and myocardial lesions was studied. Stature was not associated with any of these variables. Various measures of obesity all showed an association between obesity and the above-mentioned variables. Obese people were found to have more coronary atherosclerosis, coronary stenosis, and myocardial lesions than thin people, a difference that persisted, in a reduced form, when hypertensives and diabetics were excluded. When compared with the standardized average atherosclerosis group to exclude the effect of "wasting diseases", and when hypertensives and diabetics were excluded, neither the extent of atherosclerotic lesions nor the prevalence of coronary stenosis were increased in obese subjects. Obese men but not obese women, however, had more myocardial lesions, especially fresh myocardial infarction.
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PMID:Atherosclerosis and body build. 108 3

A new strain of rat characterized by genetic obesity, endogenous hyperlipidemia, and hypertension was obtained in this laboratory. The abnormal phenotype is inherited as a homozygous recessive trait. The animals exhibit marked hypertriglyceridemia, moderate hypercholesterolemia, and an electrophoretic pattern resembling that of human Type IV hyperlipoproteinemia. The average life-span is less than 1 year, due largely to the development of premature renal and vascular disease. The kidney lesion has both glomerulonephritic and nephrosclerotic components and is accompanied by marked proteinuria. About 12% of animals develop urinary tract calculi. The vascular disease consists of fibrous and fatty-fibrous intimal plaques, and polyarteritis. The obese animal offers a useful model for investigating abnormal lipid metabolism and the etiology and pathogenesis of atherosclerosis.
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PMID:Pathologic findings and laboratory data in a new strain of obese hypertensive rats. 117 27

In a controlled study on 121 patients with peripheral vascular disease (PVD) (75 patients with primary hyperlipoproteinemia, 15 diabetics, 31 patients without metabolic disease) the relationship between risk factors (hyperlipoproteinemia, obesity, hypertension, abnormal glucose tolerance, smoking) and the degree and localisation of sclerotic lesions was investigated by angiography. The degree was directly related in all patients to the number of risk factors, in Type IIa to cholesterol levels, in diabetics and Type IV with abnormal glucose tolerance to age. The latter patients were 5-10 years older than patients with Type IIa and showed 2 or more additional risk factors. The sclerotic lesions affected in Type IIa, less in Type IIb, predominately the pelvic vessels. Diabetics and Type IV patients showed a distal arterial involvement. The difference was significant. The degree of sclerotic lesions in arteries of the pelvis and the distal lower limb was positively correlated with the cholesterol-triglyceride ratio. Smoking aggravated the pelvic lesions in Type IV. Hypertension lead to more pronounced lesions of the distal lower limb in Type II. S-shaped tortuosities of the big vessels were shown to be typical, independent of localisation or degree.
Atherosclerosis
PMID:Primary hyperlipoproteinemias as risk factors in peripheral artery disease documented by arteriography. 119 76

Published data have suggested that hypertriglyceridemia in obesity may result from the combination of hepatic overproduction and diminished removal of triglyceride-rich lipoproteins. Diminished catabolism might be expected if tissue lipoprotein lipase activity were decreased, a finding which has been reported in biopsies of adipose tissue from obese subjects. Abnormalities in heparin-released triglyceride lipase activity (PHLA) in obesity have not been reported, however. We have examined the possibility that methods for the measurement of PHLA might have failed to reveal such a defect because of the disproportionality between plasma volume and increasing body mass in obesity. Since it is usual to administer heparin on the basis of body weight, higher plasma heparin levels would be achieved in obese individuals. We performed standard PHLA assays in lean and obese volunteers. In the obese, heparin levels were consistently higher than in lean individuals although PHLA values were similar in both. Thus, PHLA in obesity appeared to be inappropriate for the heparin levels attained in plasma. Pharmacokinetic studies suggest that a decrease in PHLA available for release by heparin rather than heparin insensitivity underlies this phenomenon.
Atherosclerosis
PMID:Abnormal post-heparin lipolytic activity in obesity. A preliminary note. 120 Nov 46

1) In 113 patients with cerebral infarction, the cause of infarction was cardiac embolism in 35, atherosclerotic thromboembolism in 45. It was either cardiac embolism or atherosclerosis but undetermined in 30. 2) Seven risk factors have been analysed. Eight patients (7 p.cent) had none of these factors. In the 105 remaining patients risk factors were: a) atrial fibrillation in 36, diagnosed in 21. Efficient treatment was applied in 1 or perhaps in 2 patients; b) High blood pressure in 39, diagnosed in 32, efficiently treated in 5; c) dyslipidemia in 42, diagnosed in 9, efficiently treated in 3; d) obesity in 50, efficiently tackled in 2; e) diabetes in 24, diagnosed in 11, efficiently treated in 2; f) hyperuricemia in 28, diagnosed in 1 with no efficient treatment; g) smoking in 44, abandonned by 1 only. 3) The high frequency of cardiac embolism is briefly commented. 4) Non diagnosis or unefficient treatment was present in a high proportion of cases. Realizing this regrettable state of affairs should result in better preventive diagnosis and treatment which, is assumed, could significantly reduce cerebral infarction.
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PMID:[Cerebral infarctions. Study of their prevention]. 120 32


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