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Results for “Syndromic obesity”

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At least 19 recordsLinked to original sources
PubMed1978

Hyperinsulinemia in obesity syndromes: its metabolic consequences and possible etiology.

Animal models with genetic or experimentally produced (lesions of hypothalamus) obesities are numerous and unlikely to ever be reduced to a single pathophysiologic entity. However, obese animals have many similar traits in common. They are all hyperinsulinemic, an abnormality that occurs early in the development of these syndromes and appears to be of prime importance in producing most of the metabolic changes observed both in the early and late phases of the obesity syndromes. In all instances, obesity is an evolutional syndrome in which the early phase is different from the later one. The early phase is principally characterized by increased hepatic very low density lipoprotein (VLDL) output, increased adipose tissue lipogenesis and VLDL uptake, hence, increased fat accretion and fat cell size. These abnormalities are secondary to hyperinsulinemia and can be reversed toward normal by normalizing circulating insulin levels. The late phase is characterized by the continuation of the disorders of the early one plus a superimposed abnormality, the insulin resistance state, that is detectable particularly at the level of adipose and muscle tissues, and eventually brings about hyperglycemia. Insulin resistance is a multifactorial pathological condition that includes at least: (a) a decrease (more or less marked) in insulin binding to target tissues that is responsible for the decrease in tissue sensitivity to the hormone; (b) intracellular defects that are probably responsible for the decreased insulin responsiveness of target tissues. The origin of hyperinsulinemia in animal obesities is still ill-defined. Lesions of the ventromedial hypothalamus (VMH) produce rapid and lasting hyperinsulinemia. Such lesions produce, in addition, increased secretion of insulin and glucagon and changes in pancreatic insulin, glucagon, and somatostatin content in subsequently perfused pancreases. The locus responsible for these effects is not defined and may actually involve a series of interrelated loci. Whatever the latter may be, one of the routes of CNS influence upon endocrine pancreas is the vagus nerve, although a humoral factor has also been claimed. The etiology of hyperinsulinemia in genetically obese animals is unknown. Genetic inheritance could bear primarily upon some hypothalamic or other CNS sites, with secondary alterations in the endocrine pancreas function, or primarily on the islets of Langerhans with possible alteration in the respective function of the A, B, and D cells with resulting excessive insulin secretion.

Animals↗
PubMed1977

Gold thioglucose obesity syndrome.

Parenteral administration of gold thioglucose to mice produces an area or necrosis in the ventromedial portion of the hypothalamus. The lesion, like lesions produced by electrocautery of this area, causes hyperphagia and consequent obesity. The glucose moiety of gold thioglucose is essential for production of the lesion. Glucose analogues (2-deoxy-glucose, sodium thioglucose and phlorizin) prevent the gold thioglucose-induced lesion, and by themselves produce a transient hyperphagia. Insulin deficiency prevents the lesion. Either adrenalectomy or hypophysectomy counteracts the effect of insulin deficiency. Electron microscopic studies, in which general necrosis is avoided by administration of aspirin before gold thioglucose or by administration of subnecrotic doses of gold thioglucose, reveal that gold thioglucose primarily affects neural elements contiguous with capillaries in the ventromedial hypothalamus. The experimental observations indicate the presence of special glucoreceptor cells in the ventromedial hypothalamus that are involved in the regulation of food intake.

Adrenalectomy↗
PubMed1978

The obesity-hypoventilation syndrome.

The triad of obesity, hypoventilation and inordinate hypersomnolence characterizes the obesity-hypoventilation syndrome. The reasons for daytime hypoventilation appear related to decreased chemical drives to breathe combined with the added physical impediment of extreme obesity. When the physiology of sleep was investigated in patients with this syndrome, intermittent nocturnal obstructive apneas were documented that produced blood gas abnormalities, arrhythmias and serious elevations of both pulmonary and systemic pressures. The obstructive apneas are due to intermittent loss of muscle tone of the tongue resulting in its prolapse against the posterior pharynx. The special importance of the obesity-hypoventilation syndrome lies in its being an example of a disorder of sleep and breathing that can appear in widely different clinical settings. Therapeutic measures include weight loss, progestational agents or permanent tracheostomy.

Apnea↗
PubMed1978

Definition, measurement, and classification of the syndromes of obesity.

The definition and risks of obesity have been reviewed and a nomogram provided for reference. Organization of information about the syndromes of obesity has been approached from several points of view. An anatomic classification has been developed, in which generalized and localized forms of fat accumulation can be separated. Hypercellularity of the adipose tissue in the childhood-onset forms of obesity is usually, but not always, present. Etiologic mechanisms are also useful in classifying obesity. This nosologic approach has been derived largely from experimental studies but has contributed significantly to understanding of pathogenetic mechanisms in man. Hypothalamic obesity is now thought to result from augmented secretion of insulin. The recessively inherited forms of obesity, on the other hand, appear to result from loss of a thermogenic system involving the ouabain-suppressible thyroid-induced (Na+ + K+) -ATPase which, in turn, accounts for the myriad of defects in these animals. Techniques of cybernetic engineering provide a third approach to classification of the syndromes of obesity. The control of body fat was analyzed as an analogy to the control of temperature in a building. These various approaches, and the new insights which they have provided for understanding the syndromes of obesity, promise to provide new pathways for pharmacologic intervention in the treatment of this problem.

Adipose Tissue↗
PubMed1977

Lowered oxygen consumption and heart rate as early symptoms of the obese-hyperglycemic syndrome in mice (ob/ob).

Latent obese-hyperglycemic mice exhibit significantly subnormal heart rate and level of oxygen consumption as early as three and eight days post-partum, respectively. Also, loss of body weight during a three-hour fasting period is detectably less extreme in obese than in normal litter mates as early as five days post-partum. Regression analysis of the differences between the latent obese and normal litter mates suggests that these symptoms begin developing at birth.

Age Factors↗
PubMed1978

Adenylate kinase activity in various organs and tissues of mice with the obese-hyperglycemic syndrome (gene symbol Ob/Ob).

The activities of adenylate kinase (ATP:AMP phosphotransferase, EC 2.7.4.3) in lyophilized cryostat sections of various organs from mice with the obese-hyperglycemic syndrome (gene symbol ob/ob) were measured fluorometrically. Skeletal and heart muscle tissues had the highest enzyme activities, i.e. 258 and 155 mmoles substrate converted per kg dry weight and per hr (MKH), respectively. Pancreatic islet specimens, which were composed mainly of B-cells, possessed the highest activitty of all parenchymatous cells studied, with 18 MKH as compared to 16 MKH for the cortical tubules of the kidney and 7 and 6 for the exocrine pancreas and liver cells, respectively. The granular layer of the cerebellum had enzyme activity of 31 MKH. The adenylate kinase activity in the B-cells was apparently not influenced by hyperglycemia since it was similar both in obese-hyperglycemic mice of different ages and in lean mice, although the blood sugar concentrations in such animals are much different.

Adenylate Kinase↗
PubMed1979

Elevated hypothalamic norepinephrine content in mice with the hereditary obese-hyperglycemic syndrome.

There is evidence that hypothalamic norepinephrine (NE) plays a role in the control of appetite in the rat. Using specific and sensitive radioenzymatic assays, we determined if there was a difference in the tissue (hypothalamus, cerebral cortex and kidney) concentration of NE or of dopamine (DA) in mice with the hereditary obese-hyperglycemic syndrome (ob/ob) and their normal weight littermates, both when they were in the rapid growth phase (2--3 months of age) and when they were mature (6--7 months of age). The concentration of NE was similar in the cerebral cortex of obese and normal mice and in the kidneys of obese and normal mice. The concentration of DA was similar in the hypothalamus of obese and normal mice. The concentration of DA was similar in the hypothalamus of obese and normal mice and in the cerebral cortex of obese and normal mice. These observations support the concept that alterations in hypothalamic NE may play a role in the obesity of ob/ob mice.

Animals↗
PubMed1976

Cushing's syndrome or obesity. Bilateral adrenal hyperplasia in a boy 10 years of age.

A rare case of the Cushing syndrome, due to bilateral adrenal hyperplasia is described. Because of generalized obesity, normal height, normal bone age and family history of obesity, a boy 10 years of age had at first been misdiagnosed as simple obesity. A reduction in height velocity, advancement of bone age and development of precocious pseudopuberty led to a more detailed biochemical investigation and to the correct diagnosis. The clinical picture can be misleading in the differential diagnosis of Cushing's disease versus simple obesity. From a comparison of reports on pediatric Cushing's syndrome, it is obvious that in most pediatric cases fat distribution differs from that of adult Cushing's syndromes. Stunted growth is reported to be more frequent, but normal and excessive height in Cushing's syndrome is not uncommon. In adrenal hyperplasia a retardation of bone age is usually expected. Interpretation of endocrine functions must take into account that simple obesity leads to secondary endocrinopathies, which are similar to the findings in Cushing's syndromes. Plasma cortisol at midnight and 12 hourly excretion of free cortisol in urine as well as overnight Dexamethasone suppression of morning plasma cortisol are judged to be good screening parameters. Plasma ACTH assays can help in the initial diagnosis and are mandatory during the follow up for an early detection of Nelson's syndrome.

Adrenal Gland Diseases↗
PubMed1978

Enzymatic studies of liver cells obtained by fine needle biopsy from mice with the obese-hyperglycemic syndrome (genesymbol ob).

In an enzymatic study of livers from obese hyperglycemic mice (obob) and their lean litter mates, microdissected freeze-dried fine needle biopsies were used. Carbohydrate, fatty acid and ketone body metabolism was examined through assays of phosphofructokinase (PFK), 3-hydroxyacyl-CoA dehydrogenase (HOADH) and D-3-hydroxybutyrate dehydrogenase (HBDH). At 2 months of age the obob-mice showed a significant increase in PFK activity as compared to their lean litter mates. No such difference was found for the activity of HOADH and HBDH. An early increase in the initial glycolysis in the livers of obob-mice might thus be one of the factors responsible for the accelerated synthesis of lipids resulting in the fatty livers of the adult obob-mice. The present results corroborate previous studies indicating no major derangement in the fatty acid and ketone body metabolism in the livers of obob-mice. In a methodological evaluation of the technique for tissue sampling and preparation, freeze-dried fine-needle punctates showed significantly higher enzyme activities of PFK and HOADH than freeze-dried liver sections or crude homogenates. Freeze-drying of fine needle biopsies appears to be a technique with good preservation of the enzyme activity. This is of significance for future metabolic studies also in humans.

3-Hydroxyacyl CoA Dehydrogenases↗
PubMed1979

The role of altered tissue norepinephrine concentration in the hereditary obese-hyperglycemic syndrome of mice.

The purpose of this study was to determine if the elevated concentration of norepinephrine in the hypothalamus of the obese-hyperglycemic mouse plays a role in the development of this syndrome. We treated normal and obese mice with the monoamine oxidase inhibitors pargyline or clorgyline for 25 weeks. This resulted in significant inhibition of monoamine oxidase in their hypothalamus, cerebral cortex, kidney, heart and epididymal fat. There was a significant increase in the norepinephrine concentration of the hypothalamus of the normal mice and the cerebral cortex of the obese mice. The obese mice receiving clorgyline had an increase in plasma glucose (313 +/- 9 mg/dl). However, the increase in tissue norepinephrine concentration did not result in increased weight gain or alterations in organ weights in the mice. Thus, the elevated hypothalamic norepinephrine concentration in obese mice is probably not the cause of their obesity.

Animals↗
PubMed1978

Morphology and enzyme activities of the retinal capillaries in mice with the obese-hyperglycaemic syndrome (gene symbol ob).

The retinal capillary bed from 67 obese-hyperglycaemic mice and 64 lean litter mates was isolated by trypsin digestion and investigated with respect to structure and enzyme activities. There was no significant difference in the ratio between numbers of endothelial and mural cells. The capillary walls did not show any obvious structural differences and microaneurysms were not observed. The retinal vessels from the obese-hyperglycaemic mice, however, displayed significantly higher activities of the enzymes hydroxyacyl-CoA-dehydrogenase, asparate aminotransferase (ASAT) and adenylate kinase than their lean litter mates. The activities of glutathione reductase, glucose-6-phosphate dehydrogenase (G-6-PDH) and phosphofructokinase were similar in the two experimental groups. It is suggested that the present data reflect early metabolic disturbances related to diabetic retinopathy.

3-Hydroxyacyl CoA Dehydrogenases↗
PubMedDate not supplied

Effects of food restriction on mice with the hereditary obese-hyperglycemic syndrome.

The purpose of this study was to compare the organ weights of obese-hyperglycemic (ob/ob) mice with the organ weights of their normal litter-mates. The absolute weights of the epididymal fat pads (white fat), interscapular fat pads (brown fat) and liver were greater in ob/ob mice than in normal mice. The weights of the kidneys and heart were similar in the 2 groups. The weights of the brain and testes were decreased in ob/ob mice when compared with normal mice. The weight gain of a second group of ob/ob mice was decreased by chronic food restriction resulting in a 26% reduction in weight when compared with ob/ob mice having unrestricted access to food. This substantially reduced the weight of the liver, but resulted in a minimal reduction in the weight of the epididymal fat pad. Food restriction did not alter the weight of the interscapular fat pads. It caused a relative reduction in kidney weight and a further absolute and relative reduction in testis weight.

Adipose Tissue↗