RELATIONSHIPS BETWEEN CALCIUM TRANSPORT AND THE LIPOLYTIC EFFECT OF SHEEP β-LIPOTROPIC HORMONE β-LPH) IN ADIPOSE TISSUE

1972 ◽  
Vol 69 (3) ◽  
pp. 507-516 ◽  
Author(s):  
M. Lis ◽  
C. Gilardeau ◽  
M. Chrétien
Keyword(s):  
Adipose Tissue ◽  
Intravenous Injection ◽  
Calcium Transport ◽  
Lipolytic Activity ◽  
Fat Cells ◽  
Tetraacetic Acid ◽  
Isolated Fat Cells ◽  
Fat Tissue ◽  
Adipose Cell ◽  
Epididymal Fat

ABSTRACT Intravenous injection of β-lipotropic hormone β-LPH) into rabbits caused a marked increase of Ca++ concentration in perirenal or epididymal fat tissue. β-LPH also increased the amount of Ca++ taken up during incubation of isolated fat cells. Incubation of fragments of rabbit fat tissue in presence of 45Ca and 3H mannitol indicated that Ca++ accumulated intra-cellularly after administration of β-LPH. In incubation media containing no Ca++, or containing Ca++ and the Ca++ sequestering agent EGTA (ethylenebis [oxyethylene nitrilo]-tetraacetic acid), β-LPH did not induce lipolysis. Addition of excess Ca++ to the EGTA containing medium restored lipolysis, whereas addition of EGTA to incubation mixtures containing Ca++ in which lipolysis in the presence of β-LPH was already proceeding stopped the lipolytic reaction. These results indicated that Ca++ is essential for lipolytic activity of β-LPH as it is for the lipolytic activity of ACTH and other structurally related peptides. Marked shift of Ca++ towards the adipose cell was correlated with β-LPH induced lipolysis.

Level of physical fitness and adipocyte lipolysis in humans

1984 ◽  
Vol 56 (5) ◽  
pp. 1157-1161 ◽  
Author(s):  
J. P. Despres ◽  
C. Bouchard ◽  
R. Savard ◽  
A. Tremblay ◽  
M. Marcotte ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Exercise Training ◽  
Lipolytic Activity ◽  
Fat Cells ◽  
Isolated Fat Cells ◽  
Fat Cell ◽  
Marathon Runners ◽  
Trained Subjects ◽  
Male Subjects ◽  
Sedentary Subjects

The present experiment was conducted to study the influence of exercise training on adipose tissue lipolytic activity and to identify the amount of training required to induce maximal adaptation in humans. Fifty-one male subjects were divided into three groups according to their training regimen: 1) sedentary subjects (SS) (n = 21); 2) trained subjects (TS) (n = 15) who had exercised during a period of 20 wk, 5 days/wk, 45 min/session; and 3) experienced marathon runners (MR) (n = 15) who ran an average of 120 km/wk for many years. Biopsies of fat were performed in the suprailiac region after an overnight fast. Adipocyte diameter (AD) and epinephrine-stimulated lipolysis ( ESL ) were assessed on collagenase-isolated fat cells. A lower AD was noted in the MR group compared with the two other groups. Basal lipolysis (BL) and ESL were significantly higher in TS and MR than in controls. Moreover, BL values were comparable in the two trained groups, whereas ESL in the TS group was higher than in the MR group. These results indicate that training increases suprailiac fat cell lipolysis, which seems to adapt maximally within about 4 mo.

scholarly journals Evidence that insulin activates casein kinase 2 in rat epididymal fat-cells and that this may result in the increased phosphorylation of an acid-soluble 22 kDa protein

1991 ◽  
Vol 279 (2) ◽  
pp. 545-551 ◽  
Author(s):  
T A Diggle ◽  
C Schmitz-Peiffer ◽  
A C Borthwick ◽  
G I Welsh ◽  
R M Denton
Keyword(s):  
Adipose Tissue ◽  
Casein Kinase ◽  
Casein Kinase 2 ◽  
Fat Cells ◽  
Isolated Fat Cells ◽  
Peptide Substrate ◽  
Heat Stable ◽  
Epididymal Fat ◽  
Rat Adipose Tissue ◽  
Fat Pads

Casein kinase 2 activity as measured by phosphorylation of the peptide substrate Arg-Arg-Arg-Glu-Glu-Glu-Thr-Glu-Glu-Glu is increased by about 50% in extracts from insulin-treated epididymal fat-pads or isolated fat-cells after purification by Mono Q chromatography. Insulin acts to increase the Vmax. of the kinase. An acid-soluble protein with an apparent subunit molecular mass of about 22 kDa appears to be a substrate for casein kinase 2. The protein possesses a number of properties in common with the acid-soluble heat-stable 22 kDa protein which exhibits increased phosphorylation in rat adipose tissue exposed to insulin.

scholarly journals Adipose Tissue Regulates Pulmonary Pathology during TB Infection

mBio ◽  
2019 ◽  
Vol 10 (2) ◽  
Author(s):  
Janeesh Plakkal Ayyappan ◽  
Usha Ganapathi ◽  
Kezia Lizardo ◽  
Christopher Vinnard ◽  
Selvakumar Subbian ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Present Report ◽  
The United States ◽  
Whole Body ◽  
World Population ◽  
Fat Cells ◽  
Fat Tissue ◽  
Disease Manifestation ◽  
Content Type ◽  
Pulmonary Pathology

ABSTRACT Tuberculosis (TB), caused by Mycobacterium tuberculosis infection, remains a major cause of mortality and morbidity worldwide. One-third of the world population is infected with M. tuberculosis, and about 15 million people with latent tuberculosis infection (LTBI) reside in the United States. An estimated 10% of individuals with LTBI are at risk of progressing to active disease. Loss of body mass, or wasting, accompanied by a significant reduction of body fat is often associated with active TB disease and is considered to be immunosuppressive and a major determinant of severity and outcome of disease. While the lungs are the primary site of M. tuberculosis infection and TB manifestation, recent reports have shown that adipose tissue serves as an important reservoir for M. tuberculosis. In this article, we investigated the association between M. tuberculosis infection, adipose tissue, and TB disease progression using a transgenic inducible “fatless” model system, the FAT-ATTAC (fat apoptosis through targeted activation of caspase 8) mouse. By selectively ablating fat tissue during M. tuberculosis infection, we directly tested the role of fat cell loss and adipose tissue physiology in regulating pulmonary pathology, bacterial burden, and immune status. Our results confirm the presence of M. tuberculosis in fat tissue after aerosol infection of mice and show that loss of fat cells is associated with an increase in pulmonary M. tuberculosis burden and pathology. We conclude that acute loss of adipose tissue during LTBI may predispose the host to active TB disease. IMPORTANCE Although the lungs are the port of entry and the predominant site of TB disease manifestation, we and others have demonstrated that M. tuberculosis also persists in adipose tissue of aerosol-infected animals and directly or indirectly alters adipose tissue physiology, which in turn alters whole-body immuno-metabolic homeostasis. Our present report demonstrates a direct effect of loss of adipocytes (fat cells) on promoting the severity of pulmonary pathogenesis during TB, advancing our understanding of the pathogenic interactions between wasting and TB activation/reactivation.

LIPOLYSIS IN CHICKEN ADIPOSE TISSUE IN VITRO

1969 ◽  
Vol 43 (2) ◽  
pp. 285-294 ◽  
Author(s):  
D. R. LANGSLOW ◽  
C. N. HALES
Keyword(s):  
Growth Hormone ◽  
Adipose Tissue ◽  
Sodium Succinate ◽  
Fat Cells ◽  
Propranolol Hydrochloride ◽  
Isolated Fat Cells ◽  
Adipose Tissue In Vitro ◽  
High Concentrations ◽  
Long Acting

SUMMARY The effects on lipolysis of various compounds have been studied in intact chicken adipose tissue and in isolated fat cells prepared from chicken adipose tissue. Glucagon stimulated lipolysis at concentrations down to 1 ng./ml. in intact pieces and 0·1 ng./ml. in isolated fat cells. The effect was enhanced by high concentrations of insulin. No anti-lipolytic effect of insulin was observed. Adrenaline, noradrenaline, porcine corticotrophin (ACTH) and long-acting ACTH were lipolytic but the effects were small and high concentrations were required. The adrenaline effect was blocked by propranolol hydrochloride. Dibutyryl 3′,5′-(cyclic)-AMP and theophylline stimulated lipolysis as did a combination of crude chicken growth hormone and hydrocortisone sodium succinate. It was concluded that the pattern of response of chicken adipose tissue was markedly different from that of the rat.

scholarly journals Effect of nutrition on subcellular localization of rat fat-cell lipoprotein lipase

1978 ◽  
Vol 172 (2) ◽  
pp. 239-245 ◽  
Author(s):  
A Vanhove ◽  
C Wolf ◽  
M Breton ◽  
M C Glangeaud
Keyword(s):  
Adipose Tissue ◽  
Lipoprotein Lipase ◽  
Plasma Membranes ◽  
Total Activity ◽  
Normal Diet ◽  
Epididymal Adipose Tissue ◽  
Fat Cells ◽  
Isolated Fat Cells ◽  
Fat Cell ◽  
Intact Tissue

This study supports the possibility for multiple subcellular forms of lipoprotein lipase. 1. The total activity of lipoprotein lipase per g of intact epididymal adipose tissue from fed rats is much higher than that from starved rats. 2. The isolated fat-cells of fed and of starved rats have lipoprotein lipase of almost the same activity per g of fat-pads. The isolated fat-cells of starved rats have a much higher proportion of total activity per g of the intact tissue than do those of fed rats. 3. Under the conditions of homogenization used, only a small proportion of the total activity per g of intact tissue from fed rats was associated with the fat layer which floated to the top of the homogenate during low-speed centrifugation. The different proportions of the specific enzyme activity found in each subcellular fraction are described. 4. Lipoprotein lipase from plasma membranes and microsomal fractions from starved and fed rats was purified by affinity chromatography. 5. The total activity of microsomal lipoprotein lipase per g of intact adipose tissue is enhanced by a normal diet. 6. In intact epididymal adipose tissue from fed rats, the activity per g of tissue of lipoprotein lipase of plasma membranes is much higher than that in the same fraction from starved rats. By contrast, the activities per g of tissue in plasma membranes obtained from starved or from fed rats by collagenase treatment were similar.

Disparate effects of ACTH(1–24) and corticosterone on lipoprotein lipase in rat adipose tissue

1987 ◽  
Vol 114 (3) ◽  
pp. 369-372 ◽  
Author(s):  
M. G. A. Baggen ◽  
H. Jansen ◽  
R. Lammers ◽  
L. Verschoor ◽  
J. C. Birkenhäger
Keyword(s):  
Adipose Tissue ◽  
Lipoprotein Lipase ◽  
Fat Tissue ◽  
Epididymal Fat ◽  
Rat Adipose Tissue ◽  
Intact Rats

ABSTRACT The effects of corticosterone and ACTH(1–24) on lipoprotein lipase (LPL) activity of rat epididymal fat tissue were studied. Hypercorticism induced by s.c. administration of 10 mg corticosterone acetate for 3 days led to a decrease in LPL activity. This decrease could be prevented by treatment of the rats simultaneously with synthetic ACTH(1–24). Adrenalectomy also reduced LPL activity. Corticosterone and ACTH(1–24) treatment had a similar effect on LPL activity in adrenalectomized and intact rats. These results indicate that ACTH(1–24) may affect adipose tissue LPL in the rat by a mechanism in which corticosterone is not involved. J. Endocr. (1987) 114, 369–372

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