Advertisement

Sign up for our daily newsletter

Advertisement

Gold thioglucose obesity rates:

Abstract Parenteral administration of gold thioglucose to mice produces an area or necrosis in the ventromedial portion of the hypothalamus. However, chow-fed GTG-obese mice have BAT mitochondria that are in a low state of thermogenic activation, and these mice fail to respond to eating a cafeteria diet for 3 wk by a normal thermogenic activation of their BAT mitochondria.

William Murphy
Thursday, March 1, 2018
Advertisement
  • Get PDF.

  • The experimental observations indicate the presence of special glucoreceptor cells in the ventromedial hypothalamus that are involved in the regulation of food intake.

  • View Metrics.

  • Dietary influences on BAT thermogenic function are, however, defective in the GTG-obese mouse at least during the dynamic phase of its obesity.

  • Ablation of the adrenal glands after the administration of GTG prevented the onset and development of hyperphagia and obesity.

Publication types

The tissue gold thioglucose obesity rates normally when the mice adapt to cafeteria feeding or to cold 8 degrees C. Acute exposure to cold causes a fairly normal thermogenic activation of BAT mitochondria of GTG-obese mice, both in dynamic and static phases of their obesity. It is concluded that BAT of the GTG-obese mouse is inherently functional, as is control of its thermogenic function and growth during cold exposure and cold acclimation.

The tissue grows normally when the mice adapt to cafeteria feeding or to cold 8 degrees C. Substances Aurothioglucose. Insulin gold thioglucose obesity rates prevents the lesion. Either adrenalectomy or hypophysectomy counteracts the effect of insulin deficiency. The resulting failure of diet-induced thermogenesis would be expected to contribute to the known high metabolic efficiency of the GTG-obese mouse and, together with the hyperphagia, to the obesity induced by GTG. Publication types Research Support, U. The experimental observations indicate the presence of special glucoreceptor cells in the ventromedial hypothalamus that are involved in the regulation of food intake.

ALSO READ: Definition Of Child Overweight And Obesity Worldwide

Socio ecological model cdc obesity rates experimental observations indicate the presence yold special glucoreceptor cells in the ventromedial hypothalamus that are involved in the regulation of food intake. The lesion, like lesions produced by electrocautery of this area, causes hyperphagia and consequent obesity. More prolonged cafeteria feeding for wk, into the static phase of obesity, is associated with thermogenic activation of BAT mitochondria of GTG-obese mice. The tissue grows normally when the mice adapt to cafeteria feeding or to cold 8 degrees C. It is concluded that BAT of the GTG-obese mouse is inherently functional, as is control of its thermogenic function and growth during cold exposure and cold acclimation.

The resulting failure of diet-induced thermogenesis would be expected to contribute to the known high metabolic efficiency of the GTG-obese mouse and, together with the hyperphagia, gold thioglucose obesity rates the obesity induced by GTG. The lesion, like lesions produced by electrocautery of this area, causes hyperphagia and consequent obesity. Gov't, P. The capacity of GTG-obese mice to respond to noradrenaline norepinephrine by an increase in metabolic rate is greater than that of lean mice and is further enhanced by cold acclimation. Dietary influences on BAT thermogenic function are, however, defective in the GTG-obese mouse at least during the dynamic phase of its obesity. More prolonged cafeteria feeding for wk, into the static phase of obesity, is associated with thermogenic activation of BAT mitochondria of GTG-obese mice. Gold thioglucose GTG -obese mice have a larger than normal amount of brown adipose tissue BAT with ultrastructurally normal mitochondria.

Get Access To This Article

Previous studies from our laboratory suggested that adrenal hormones may participate, directly or indirectly, in the hypothalamic mechanism involved in the regulation of food intake. View full article. Proc Soc Exp Biol Med. Mustafa Sahin Nilgun Demirag Guvener.

Pashko, PhD, Arthur G. Similar Articles To arrive at the top five similar articles we use a word-weighted algorithm to compare words from the Title and Abstract of each citation. Copyright notice. BioStudies: supplemental material and supporting data.

  • American Diabetes Association Journals Discover the latest diabetes research published by the journals from the American Diabetes Association.

  • More prolonged cafeteria feeding for wk, into the static phase of obesity, is associated with thermogenic activation of BAT mitochondria of GTG-obese mice. Glucose analogues 2-deoxy-glucose, sodium thioglucose and phlorizin prevent the gold thioglucose-induced lesion, and by themselves produce a transient hyperphagia.

  • Research Article November 01

  • Publication types Research Support, U.

Receive exclusive offers and updates from Oxford Academic. Volume I agree, dismiss this banner. Skip Nav Destination Article Navigation. Remission of insulin resistant diabetes in two patients with anti-insulin receptor antibodies opens in new tab. Sign In.

More prolonged cafeteria feeding for wk, into the static phase of obesity, is associated with thermogenic activation of BAT mitochondria of GTG-obese mice. Substances Tates. Abstract Gold thioglucose GTG -obese mice have a larger than normal amount of brown adipose tissue BAT with ultrastructurally normal mitochondria. The glucose moiety of gold thioglucose is essential for production of the lesion. Abstract Parenteral administration of gold thioglucose to mice produces an area or necrosis in the ventromedial portion of the hypothalamus. It is concluded that BAT of the GTG-obese mouse is inherently functional, as is control of its thermogenic function and growth during cold exposure and cold acclimation. Publication types Research Support, U.

MeSH terms

Open in a separate window. Email alerts Article activity alert. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide.

It is concluded that BAT of the GTG-obese mouse is inherently functional, as is control of its thermogenic function and growth during cold exposure and cold acclimation. Gold thioylucose GTG -obese mice have rates larger than normal amount of brown adipose tissue BAT with ultrastructurally normal mitochondria. The glucose moiety of gold thioglucose is essential for production of the lesion. The experimental observations indicate the presence of special glucoreceptor cells in the ventromedial hypothalamus that are involved in the regulation of food intake. The lesion, like lesions produced by electrocautery of this area, causes hyperphagia and consequent obesity. Either adrenalectomy or hypophysectomy counteracts the effect of insulin deficiency. Parenteral administration of gold thioglucose to mice produces an area or necrosis in the ventromedial portion of the hypothalamus.

Gold thioglucose obesity rates J 3 : — Volume These results indicate that increased lipogenesis in GTG-injected mice may be due to an increase in insulin concentration after feeding and that insulin resistance assessed by lipogenic response to insulin release is apparent in BAT before WAT and liver. In WAT, lipogenesis after feeding was highest weeks after GTG injection, and in liver, lipid synthesis in fed obese mice was greatest at weeks after the induction of obesity.

Fecal microbiota transplantation from high caloric-fed donors alters glucose metabolism in recipient mice, independently of adiposity or exercise status. Adipose tissue fatty acid chain gold thioglucose obesity rates and mono-unsaturation increases with obesityy and insulin resistance. Cited by: 0 articles PMID: The dose-response characteristics of several glucose-utilizing tissues brain, heart, white adipose tissue, brown adipose tissue, and quadriceps muscle to a single injection of insulin have been compared in control mice and mice made obese with a single injection of gold thioglucose GTG. Download all slides. As expected, damage to the ventromedial hypothalamus by GTG was followed by hyperphagia and obesity.

Publication types

More prolonged cafeteria feeding for wk, into the static phase of obesity, is associated with thermogenic activation of BAT mitochondria of GTG-obese mice. However, chow-fed GTG-obese mice have BAT mitochondria that are in a low state of thermogenic activation, and these mice fail to respond to eating a cafeteria diet for 3 wk by a normal thermogenic activation of their BAT mitochondria. The tissue grows normally when the mice adapt to cafeteria feeding or to cold 8 degrees C. 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.

An hypothesis on rates aetiology of obesity: dysfunction of the central nervous system as a primary cause. Longitudinal study on the establishment of insulin resistance in hypothalamic obese mice. The administration of desoxycorticosterone not only failed to restore the hyperphagia and obesity in these mice but, rather, led to a suppression of food intake, weight loss, and death. This website requires cookies, and the limited processing of your personal data in order to function.

ALSO READ: Overweight And Obesity Causes Overeating

The experimental observations indicate the presence of special glucoreceptor cells in the ventromedial hypothalamus that are involved in the regulation of food intake. Insulin deficiency prevents the lesion. The resulting failure of diet-induced thermogenesis would be expected to contribute to the known high metabolic efficiency of the GTG-obese mouse and, together with the hyperphagia, to the obesity induced by GTG. Gold thioglucose GTG -obese mice have a larger than normal amount of brown adipose tissue BAT with ultrastructurally normal mitochondria. The glucose moiety of gold thioglucose is essential for production of the lesion. Publication types Research Support, U.

Insulin deficiency prevents the lesion. It is concluded that BAT of the GTG-obese mouse gold thioglucose obesity rates inherently functional, as is control of its thermogenic tbioglucose and growth during cold exposure and cold acclimation. Glucose analogues 2-deoxy-glucose, sodium thioglucose and phlorizin prevent the gold thioglucose-induced lesion, and by themselves produce a transient hyperphagia. More prolonged cafeteria feeding for wk, into the static phase of obesity, is associated with thermogenic activation of BAT mitochondria of GTG-obese mice. Substances Aurothioglucose. Gov't, P.

Close Modal. Uncoupling protein 1 is necessary for norepinephrine-induced glucose utilization in brown adipose tissue. Tracing insights into de novo lipogenesis in liver and adipose tissues. Skip Nav Destination Article Navigation.

The resulting failure of thioglucoee thermogenesis would be expected to contribute to the known high metabolic efficiency of rates GTG-obese mouse and, together with the hyperphagia, to the obesity induced by GTG. Substances Aurothioglucose. The lesion, like lesions produced by electrocautery of this area, causes hyperphagia and consequent obesity. Abstract Gold thioglucose GTG -obese mice have a larger than normal amount of brown adipose tissue BAT with ultrastructurally normal mitochondria. 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.

Both lean and obese mice had one main thiogluucose period, from to h. Cited by: 4 articles PMID: Related Papers. Development of VMH obesity: in vivo insulin secretion and tissue insulin sensitivity. Liver and peripheral tissue glycogen metabolism in obese mice: effect of a mixed meal. Abstract Previous studies from our laboratory suggested that adrenal hormones may participate, directly or indirectly, in the hypothalamic mechanism involved in the regulation of food intake. The loss of diet-induced thermogenesis in brown adipose tissue as a result of the hypothalamic lesion in GTG-obese mice could be a major cause

More prolonged cafeteria feeding for wk, into the static phase of obesity, is associated with thermogenic activation of BAT mitochondria of GTG-obese mice. However, chow-fed GTG-obese gold thioglucose obesity rates have BAT mitochondria that are in a low state of thermogenic activation, and these mice fail to respond to eating a cafeteria diet for 3 wk by a normal thermogenic activation of their BAT mitochondria. The resulting failure of diet-induced thermogenesis would be expected to contribute to the known high metabolic efficiency of the GTG-obese mouse and, together with the hyperphagia, to the obesity induced by GTG.

GB DheaCaloric restriction obesity rates, Tumor initiatorsObese mouse. Sign in Don't gld have an account? J Nutr Biochem11 201 Feb Recent history Saved searches. This article has been cited by other articles in PMC. In vivo insulin sensitivity of the pyruvate dehydrogenase complex in tissues of the rat.

ALSO READ: Hypothyroidism Hard To Get Out Of Bed

Vanner MA. Proc Soc Exp Biol Med. Get PDF. Abstract This study socio ecological model cdc obesity rates undertaken to determine whether a reduction in body weight in laboratory mice by regimens that appear to delay the rate of aging i. By continuing to use our website, you are agreeing to our privacy policy.

The capacity of GTG-obese mice to respond to noradrenaline norepinephrine by an increase in gold thioglucose obesity rates rate is greater than that of lean obesith and is further enhanced by cold acclimation. Abstract Parenteral administration of gold thioglucose to mice produces an area or necrosis in the ventromedial portion of the hypothalamus. The tissue grows normally when the mice adapt to cafeteria feeding or to cold 8 degrees C. Substances Aurothioglucose. The glucose moiety of gold thioglucose is essential for production of the lesion.

The tissue grows normally when the mice adapt to cafeteria feeding or to cold 8 degrees C. Glucose analogues 2-deoxy-glucose, sodium thioglucose and phlorizin prevent the gold thioglucose-induced lesion, and by themselves produce a transient hyperphagia. Gov't, P.

Acute exposure to cold causes a fairly normal thermogenic activation of BAT mitochondria of GTG-obese mice, both in dynamic and static phases of their obesity. The capacity of GTG-obese mice to respond to noradrenaline norepinephrine by an increase in metabolic rate is greater than that of lean mice and is further enhanced by cold acclimation. Either adrenalectomy or hypophysectomy counteracts the effect of insulin deficiency. Substances Aurothioglucose. 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. Parenteral administration of gold thioglucose to mice produces an area or necrosis in the ventromedial portion of the hypothalamus. The tissue grows normally when the mice adapt to cafeteria feeding or to cold 8 degrees C.

ALSO READ: Obesity And Mobility

Gold thioglucose obesity rates muscle-specific overproduction of constitutively activated c-Jun N-terminal kinase JNK induces insulin resistance in mice. The loss of diet-induced thermogenesis in brown adipose tissue as a result of the hypothalamic lesion in GTG-obese mice could be a major cause Affiliations 1 author 1. Sign In or Create an Account. Europe PMC requires Javascript to function effectively.

Publication types Research Support, U. Thioglucosd capacity of GTG-obese mice to respond to noradrenaline norepinephrine by an increase in metabolic rate is greater than that of lean mice and is further enhanced by cold acclimation. Either adrenalectomy or hypophysectomy counteracts the effect of insulin deficiency. Parenteral administration of gold thioglucose to mice produces an area or necrosis in the ventromedial portion of the hypothalamus. Insulin deficiency prevents the lesion.

Google Scholar. Biochem J 1 November ; 3 : — Cite Cite Laura L. Substances Aurothioglucose Desoxycorticosterone Gold Cortisone.

  • Brain 2-DG phosphorylation was insulin independent in control and obese animals. Long-term cytogenetic follow-up studies on humans after internal and external exposures to ionizing radiation.

  • More prolonged cafeteria feeding for wk, into the static phase of obesity, is associated with thermogenic activation of BAT mitochondria of GTG-obese mice.

  • Cancer stem cell phosphatases.

  • Download all slides.

I agree, dismiss this banner. There was also a 3-fold increase in cardiac Thioglucosr activity and a 3-fold increase in hepatic lipogenesis in the control mice, but little change in hepatic PDHC activity. Sign In Reset password. Eating produced no change in serum glucose of control mice but there was a significant rise in serum insulin and triacylglycerols. You do not currently have access to this article.

However, chow-fed GTG-obese mice have BAT mitochondria that are in a low state of thermogenic activation, and these mice fail to respond to eating a cafeteria diet for 3 wk by a normal thermogenic activation of their BAT mitochondria. The glucose moiety of gold thioglucose is essential for production of the lesion. Abstract Parenteral administration of gold thioglucose to mice produces an area or necrosis in the ventromedial portion of the hypothalamus. Gov't, P. Dietary influences on BAT thermogenic function are, however, defective in the GTG-obese mouse at least during the dynamic phase of its obesity.

Gold thioglucose obesity rates influence of environmental temperature on the proportion of whole-body fatty acid synthesis in brown adipose tissue and the liver. Evidence for a high fatty acid synthesis activity in interscapular brown adipose tissue of genetically obese Zucker rats. Advanced Search. GTG-obese mice were hyperglycaemic, hyperinsulinaemic and hypertriglyceridaemic at all times studied, with significant increases in these parameters being seen in response to eating. Skip Nav Destination Article Navigation. Maung Khant Marianne Elston.

Related Feeds. Sign in Don't already have an account? Autoimmune forms of hypoglycemia.

The experimental observations indicate the presence of special glucoreceptor cells in the ventromedial hypothalamus that are involved in the regulation of food intake. Thioglucode Parenteral administration of gold thioglucose to mice produces an area or necrosis in the ventromedial portion of the hypothalamus. The resulting failure of diet-induced thermogenesis would be expected to contribute to the known high metabolic efficiency of the GTG-obese mouse and, together with the hyperphagia, to the obesity induced by GTG. The glucose moiety of gold thioglucose is essential for production of the lesion.

The resulting failure of diet-induced thermogenesis would be expected to contribute to the known high metabolic efficiency of the GTG-obese gold thioglucose obesity rates ratess, together with the hyperphagia, to the obesity induced by GTG. The experimental observations indicate the presence of special glucoreceptor cells in the ventromedial hypothalamus that are involved in the regulation of food intake. However, chow-fed GTG-obese mice have BAT mitochondria that are in a low state of thermogenic activation, and these mice fail to respond to eating a cafeteria diet for 3 wk by a normal thermogenic activation of their BAT mitochondria. Substances Aurothioglucose. Insulin deficiency prevents the lesion.

However, chow-fed GTG-obese mice have BAT mitochondria that are in a low state of thermogenic activation, and these mice gold thioglucose obesity rates to respond to eating a cafeteria diet for 3 wk by a normal thermogenic activation of their BAT mitochondria. Either adrenalectomy or hypophysectomy counteracts the effect of insulin deficiency. The experimental observations indicate the presence of special glucoreceptor cells in the ventromedial hypothalamus that are involved in the regulation of food intake. Publication types Research Support, U.

Glucose analogues 2-deoxy-glucose, sodium thioglucose and phlorizin prevent the socio ecological model cdc obesity rates thioglucose-induced lesion, and by themselves produce a transient hyperphagia. Parenteral administration of gold thioglucose to mice produces an area or necrosis in the ventromedial portion of the hypothalamus. Insulin deficiency prevents the lesion. Abstract Parenteral administration of gold thioglucose to mice produces an area or necrosis in the ventromedial portion of the hypothalamus.

  • Volume This article is also available for rental through DeepDyve.

  • Either adrenalectomy or hypophysectomy counteracts the effect of insulin deficiency. Publication types Research Support, U.

  • Jeanrenaud B.

  • All Issues. DheaCaloric restrictionTumor initiatorsObese mouse.

  • Sign in Don't already have an Oxford Academic account?

Brown adipose tissue activity in hypophysectomized rats: involvement of sympathetic system opens in new tab. Implications for obesity. Glucose utilization in vivo and insulin-sensitivity of rat brown adipose tissue in various physiological and pathological conditions. External link.

The capacity of GTG-obese mice to respond to noradrenaline norepinephrine by an increase in metabolic rate is greater than ohesity of lean mice and is further enhanced by cold acclimation. Substances Aurothioglucose. The experimental observations indicate the presence of special glucoreceptor cells in the ventromedial hypothalamus that are involved in the regulation of food intake. The lesion, like lesions produced by electrocautery of this area, causes hyperphagia and consequent obesity.

Mustafa Sahin Nilgun Demirag Guvener. Full text links Read article at publisher's site DOI : Cancer stem cell phosphatases. Data Data behind the article This data has been text mined from the article, or deposited into data resources.

The resulting failure of diet-induced thermogenesis would be expected to contribute to the known high metabolic efficiency of the GTG-obese mouse and, together with the hyperphagia, to the obesity induced by GTG. Publication types Research Support, U. The experimental observations indicate the presence of special glucoreceptor cells in the ventromedial hypothalamus that are involved in the regulation of food intake. 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. Either adrenalectomy or hypophysectomy counteracts the effect of insulin deficiency.

American Diabetes Association Journals Discover the latest diabetes research published by the journals from the American Diabetes Association. The simultaneous rise of hepatic PDHC thikglucose, lipogenesis and serum triacylglycerols in GTG-obese mice suggests an increased utilization of glucose for lipogenesis. Acute effects in vivo of anti-insulin serum on rates of fatty acid synthesis and activities of acetyl-coenzyme A carboxylase and pyruvate dehydrogenase in liver and epididymal adipose tissue of fed rats. Lipogenesis in BAT from GTG mice was double that of control mice for the first 2 weeks, but subsequently decreased to near control values. I agree, dismiss this banner. Brown adipose tissue thermogenesis and obesity. Purchase Subscription prices and ordering Short-term Access To purchase short term access, please sign in to your Oxford Academic account above.

The largest decrease in insulin sensitivity in GTG-obese mice was observed in brown adipose tissue. Vanner MA. Pashko, PhDLaura L.

Article Navigation. Please review our privacy policy. Cancer stem cell phosphatases. Gov't, Non-P. Stimulation of hypothalamic nuclei has differential effects on lipid synthesis in brown and white adipose tissue.

Dietary influences on BAT thermogenic function are, however, defective in the GTG-obese mouse at least during the dynamic phase of its obesity. Either adrenalectomy or hypophysectomy counteracts the effect of insulin deficiency. However, chow-fed GTG-obese mice have BAT mitochondria that are in a low state of thermogenic activation, and these mice fail to respond to eating a cafeteria diet for 3 wk by a normal thermogenic activation of their BAT mitochondria. Gov't, P. It is concluded that BAT of the GTG-obese mouse is inherently functional, as is control of its thermogenic function and growth during cold exposure and cold acclimation.

The tissue grows normally when the mice adapt to cafeteria feeding or to cold 8 degrees C. Ratea exposure to cold causes a fairly obesity rates thermogenic activation of BAT mitochondria of GTG-obese mice, both in dynamic and static phases of their obesity. Dietary influences on BAT thermogenic function are, however, defective in the GTG-obese mouse at least during the dynamic phase of its obesity. 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. Glucose analogues 2-deoxy-glucose, sodium thioglucose and phlorizin prevent the gold thioglucose-induced lesion, and by themselves produce a transient hyperphagia.

Fatty acid synthesis in mouse brown adipose tissue. Brown adipose tissue activity in hypophysectomized rats: involvement of sympathetic system opens in new tab. Associated Data Supplementary Materials. Semin Cell Dev Biol, 19 Mar Eating produced no change in serum glucose of control mice but there was a significant rise in serum insulin and triacylglycerols.

Sign In Forgot password? Diabetes Care. The loss of diet-induced thermogenesis in brown adipose tissue as a result of the hypothalamic lesion in GTG-obese mice could be a major cause Open in a separate window. Biochim Biophys Acta. Brown adipose tissue thermogenesis and obesity.

ALSO READ: Low Circulating Vitamin D In Obesity Facts

The capacity of GTG-obese mice to respond to noradrenaline norepinephrine by an increase in metabolic rate is greater than that of lean mice and gold thioglucose further enhanced by cold acclimation. Gov't, P. Insulin deficiency prevents the lesion. Substances Aurothioglucose. The resulting failure of diet-induced thermogenesis would be expected to contribute to the known high metabolic efficiency of the GTG-obese mouse and, together with the hyperphagia, to the obesity induced by GTG. The lesion, like lesions produced by electrocautery of this area, causes hyperphagia and consequent obesity. Dietary influences on BAT thermogenic function are, however, defective in the GTG-obese mouse at least during the dynamic phase of its obesity.

However, chow-fed GTG-obese mice have Rates mitochondria that are in a low state of thermogenic activation, and these mice fail to respond to eating a cafeteria diet for 3 wk by a normal thermogenic activation of their BAT mitochondria. Dietary influences on BAT thermogenic function are, however, defective in the GTG-obese mouse at least during the dynamic phase of its obesity. Parenteral administration of gold thioglucose to mice produces an area or necrosis in the ventromedial portion of the hypothalamus. Acute exposure to cold causes a fairly normal thermogenic activation of BAT mitochondria of GTG-obese mice, both in dynamic and static phases of their obesity. Abstract Parenteral administration of gold thioglucose to mice produces an area or necrosis in the ventromedial portion of the hypothalamus.

Eating produced gold thioglucose obesity rates change in cardiac PDHC activity, rrates there was a 5-fold increase in hepatic PDHC activity, paralleled by a fold increase in hepatic lipogenesis. The fatty acid synthesis after a meal was higher in all tissues of GTG-treated mice on a total-tissue basis, but the magnitude of this increase varied, depending on the tissue and the time after the initiation of obesity. Either your web browser doesn't support Javascript or it is currently turned off. Cooney GJ 1 .

Oxford University Press is a department of the University of Oxford. Issue Section:. The diurnal pattern of the activity of the pyruvate dehydrogenase complex PDHC was studied in the heart and liver of gold-thioglucose GTG -obese mice and age-matched controls. In vivo insulin sensitivity of the pyruvate dehydrogenase complex in tissues of the rat. Liver and peripheral tissue glycogen metabolism in obese mice: effect of a mixed meal. Permissions Icon Permissions. Jeanrenaud B.

Publication types Research Support, U. However, chow-fed Fhioglucose mice have BAT mitochondria that are in a low state of thermogenic activation, and these mice fail to respond to eating a cafeteria diet for 3 wk by a normal thermogenic activation of their BAT mitochondria. Either adrenalectomy or hypophysectomy counteracts the effect of insulin deficiency. Abstract Gold thioglucose GTG -obese mice have a larger than normal amount of brown adipose tissue BAT with ultrastructurally normal mitochondria. The lesion, like lesions produced by electrocautery of this area, causes hyperphagia and consequent obesity. Parenteral administration of gold thioglucose to mice produces an area or necrosis in the ventromedial portion of the hypothalamus. Substances Aurothioglucose.

Abstract Parenteral administration of gold thioglucose gold thioglucose obesity rates mice produces an raates or necrosis in the ventromedial portion of the hypothalamus. Either adrenalectomy or hypophysectomy counteracts the effect of insulin deficiency. Publication types Research Support, U. The tissue grows normally when the mice adapt to cafeteria feeding or to cold 8 degrees C.

The tissue grows normally when the mice adapt to cafeteria feeding rwtes to cold 8 degrees C. Gov't, P. The capacity of GTG-obese mice to respond to noradrenaline norepinephrine by an increase in metabolic rate is greater than that of lean mice and is further enhanced by cold acclimation. Substances Aurothioglucose.

  • S Takayama-Hasumi M Kasuga. Diabetologia28 801 Aug

  • Substances Aurothioglucose.

  • A comparison of extrahepatic lipogenesis from a small glucose meal in obob and gold thioglucose obese mice fed low- or high-fat diets with or without the addition of Deltabeta-taurocholenic acid. Williams PF .

Mustafa Sahin Nilgun Demirag Guvener. Differences in lipogenesis in tissues of control and gold-thioglucose obese mice gold thioglucose obesity rates an isocaloric meal. To arrive at the top five similar articles we use a word-weighted algorithm to compare words from the Title and Abstract of each citation. Citing articles via Web of Science

M Goubern R Portet. Thiogludose Navigation. Effect of adrenalectomy on glucose tolerance and lipid cdc obesity in gold-thioglucose obese mice. Mustafa Sahin Nilgun Demirag Guvener. The activity of the pyruvate dehydrogenase complex in heart and liver from mice during the development of obesity and insulin resistance. This article has been cited by other articles in PMC. Vanner MA .

Read more about:

Sidebar1?
Sidebar2?