scholarly journals Responses of Adipose and Muscle Lipoprotein Lipase to Chronic Infection and Subsequent Acute Lipopolysaccharide Challenge

2002 ◽  
Vol 9 (4) ◽  
pp. 771-776 ◽  
Author(s):  
Frédéric Picard ◽  
Denis Arsenijevic ◽  
Denis Richard ◽  
Yves Deshaies
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Weight Gain ◽  
Energy Balance ◽  
Lipoprotein Lipase ◽  
Neospora Caninum ◽  
Body Weight Gain ◽  
Acute Response ◽  
Lps Treatment

ABSTRACT Infection of male Swiss Webster mice with Toxoplasma gondii or Neospora caninum leads to long-term alterations in energy balance. Following an initial 20 to 30% weight loss in all T. gondii-infected mice, half of the animals regain most of the lost weight (gainers), whereas the others maintain their low body weight (nongainers). Infection with N. caninum does not elicit weight loss. Lipoprotein lipase (LPL), the enzyme responsible for plasma triglyceride (TG) clearance and partitioning among tissues, is under tissue-specific modulation associated with energy balance. It is also a major determinant of infection-induced hypertriglyceridemia. This study aimed to assess the long-term modulation of adipose and muscle LPL activity in mice infected with T. gondii or N. caninum, to evaluate the effects of subsequent acute lipopolysaccharide (LPS) administration, and to relate LPL modulation in these conditions with infection-related changes in body weight gain. Twenty-eight days after infection, LPL activity in muscle of both gainer and nongainer T. gondii-infected mice was reduced by 40 to 50% compared with the levels in controls and N. caninum-infected mice, whereas LPL activity in adipose depots remained unchanged in all infected groups compared to the level in controls. LPS (from Escherichia coli, 100 ng/kg) injection induced a global reduction in adipose LPL in all groups, as assessed 90 min later. In both T. gondii-infected subgroups, muscle LPL was not further reduced by LPS treatment, whereas it was decreased by 40 to 50% in muscles of control and N. caninum-infected mice. Pre-LPS TG levels in plasma were similar in all groups. LPS greatly increased TG levels in plasma in both control and N. caninum-infected animals, whereas it did not alter those of T. gondii-infected gainer or nongainer animals. These results show that (i) independently of the extent of postinfection weight gain, long-term infection with T. gondii chronically reduces muscle LPL, which becomes unresponsive to acute endotoxemia; (ii) modulation of tissue LPL activity during chronic T. gondii infection favors TG partitioning towards adipose tissue; and (iii) skeletal muscle LPL is a key determinant of the acute response of triglyceridemia to LPS.

Tracking human fat turnover with carbon dating

2019 ◽  
Vol 11 (511) ◽  
pp. eaaz4961
Author(s):  
Ming Yang
Keyword(s):  
Bariatric Surgery ◽  
Weight Loss ◽  
Body Weight ◽  
Adipose Tissue ◽  
Weight Gain ◽  
Body Weight Gain ◽  
Weight Loss Maintenance ◽  
Carbon Dating ◽  
Lipid Turnover

Lipid turnover in adipose tissue is important in long-term body weight gain and weight loss maintenance after bariatric surgery in humans.

Insulin and central regulation of spontaneous fattening and weight loss

1985 ◽  
Vol 249 (2) ◽  
pp. R203-R208
Author(s):  
R. B. Melnyk ◽  
J. M. Martin
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Weight Gain ◽  
Energy Balance ◽  
Binding Capacity ◽  
Insulin Receptors ◽  
Insulin Binding ◽  
Strong Positive Correlation ◽  
Central Regulation ◽  
Isolated Pancreatic Islets

Insulin binding to receptors in a partially purified hypothalamic membrane preparation is altered by prolonged starvation. To define further the relationship between hypothalamic insulin binding and energy balance, we studied the Richardson's ground squirrel, a hibernator that exhibits spontaneous 6- to 8-mo body weight cycles when kept in constant conditions. Isolated pancreatic islets from squirrels killed during the weight gain phase had greater glucose-stimulated insulin secretion than those from weight loss phase animals, and adipocytes showed significantly greater glucose incorporation into total lipid in response to insulin. Differences in lipogenesis were not attributable to changes in insulin-binding capacity. Hypothalamic tissue from weight gain phase animals bound more insulin than that from weight loss phase animals. Maximal binding was correlated with pancreatic islet responsiveness and maximal insulin-stimulated lipogenesis. The strong positive correlation between peripheral metabolic events associated with spontaneous alterations in energy balance and the binding kinetics of hypothalamic insulin receptors suggests that insulin may play an important role in the central regulation of body weight.

Effect of exercise training on energy balance of orchidectomized rats

1989 ◽  
Vol 257 (3) ◽  
pp. R550-R555 ◽  
Author(s):  
S. Rivest ◽  
J. Landry ◽  
D. Richard
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Energy Balance ◽  
Cytochrome C ◽  
Exercise Training ◽  
Protein Content ◽  
Cytochrome C Oxidase ◽  
Oxidase Activity ◽  
Body Weight Gain ◽  
Energy Gain

The purpose of the present study was to investigate both the respective and interactive roles of exercise training and testosterone on energy balance. Male rats were divided into sedentary and exercise-trained groups. Each group formed was further divided into a sham-operated group, an orchidectomized group, or an orchidectomized group treated with testosterone. Rats were exercised on a motor-driven treadmill for 1 h/day over 28 consecutive days, after which rats were killed. Energy balance measurements, body composition analyses, and serum testosterone assay were then performed. The weight, protein content, and cytochrome-c oxidase activity of interscapular brown adipose tissue (IBAT) were also measured. Results indicate that total food intake, final body weight, and body weight gain were generally lower in exercise-trained rats than in sedentary animals. In orchidectomized rats treated with testosterone, gains of both fat and protein were lower in exercise-trained than in sedentary animals. There was no difference in metabolizable energy intake and body energy gain between trained and sedentary rats that underwent orchidectomy without replacement therapy. In orchidectomized groups of rats, energy gain was lower in trained rats that were treated with testosterone than in those that did not receive any treatment. Furthermore, in trained orchidectomized rats treated with testosterone, both energetic efficiency and energy density of body weight gain were lower than those of trained orchidectomized rats that were not treated. Finally, a significant reduction in IBAT weight was observed in exercise-trained animals, whereas neither exercise nor the various hormonal manipulations affected IBAT protein content and cytochrome-c oxidase activity.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Combined Deletion of Y1, Y2, and Y4 Receptors Prevents Hypothalamic Neuropeptide Y Overexpression-Induced Hyperinsulinemia despite Persistence of Hyperphagia and Obesity

Endocrinology ◽  
2006 ◽  
Vol 147 (11) ◽  
pp. 5094-5101 ◽  
Author(s):  
En-Ju D. Lin ◽  
Amanda Sainsbury ◽  
Nicola J. Lee ◽  
Dana Boey ◽  
Michelle Couzens ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Neuropeptide Y ◽  
Energy Homeostasis ◽  
Viral Vector ◽  
Body Weight Gain ◽  
Hormonal Changes ◽  
Obesity Syndrome ◽  
Y Receptors

Neuropeptide Y (NPY) is a key regulator of energy homeostasis and is implicated in the development of obesity and type 2 diabetes. Whereas it is known that hypothalamic administration of exogenous NPY peptides leads to increased body weight gain, hyperphagia, and many hormonal and metabolic changes characteristic of an obesity syndrome, the Y receptor(s) mediating these effects is disputed and unclear. To investigate the role of different Y receptors in the NPY-induced obesity syndrome, we used recombinant adeno-associated viral vector to overexpress NPY in mice deficient of selective single or multiple Y receptors (including Y1, Y2, and Y4). Results from this study demonstrated that long-term hypothalamic overexpression of NPY lead to marked hyperphagia, hypogonadism, body weight gain, enhanced adipose tissue accumulation, hyperinsulinemia, and other hormonal changes characteristic of an obesity syndrome. NPY-induced hyperphagia, hypogonadism, and obesity syndrome persisted in all genotypes studied (Y1−/−, Y2−/−, Y2Y4−/−, and Y1Y2Y4−/− mice). However, triple deletion of Y1, Y2, and Y4 receptors prevented NPY-induced hyperinsulinemia. These findings suggest that Y1, Y2, and Y4 receptors under this condition are not crucially involved in NPY’s hyperphagic, hypogonadal, and obesogenic effects, but they are responsible for the central regulation of circulating insulin levels by NPY.

Pioglitazone-induced body weight gain is prevented by combined administration with the lipoprotein lipase activator NO-1886

2011 ◽  
Vol 668 (3) ◽  
pp. 486-491 ◽  
Author(s):  
Masataka Kusunoki ◽  
Kazuhiko Tsutsumi ◽  
Daisuke Sato ◽  
Aki Nakamura ◽  
Satoshi Habu ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Lipoprotein Lipase ◽  
Body Weight Gain ◽  
Combined Administration

Early nutritional changes induce sexually dimorphic long-term effects on body weight gain and the response to sucrose intake in adult rats

Metabolism ◽  
2012 ◽  
Vol 61 (6) ◽  
pp. 812-822 ◽  
Author(s):  
Esther Fuente-Martín ◽  
Miriam Granado ◽  
Cristina García-Cáceres ◽  
Miguel A. Sanchez-Garrido ◽  
Laura M. Frago ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Body Weight Gain ◽  
Sexually Dimorphic ◽  
Sucrose Intake ◽  
Long Term Effects ◽  
Adult Rats ◽  
Nutritional Changes

Long-term reductions in GH, insulin-like growth factor-I and body weight gain in rats treated neonatally with antibodies to rat GH

1990 ◽  
Vol 124 (3) ◽  
pp. 381-386 ◽  
Author(s):  
M. J. Gardner ◽  
D. J. Flint
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Growth Factor ◽  
Body Weight Gain ◽  
Female Rats ◽  
Serum Prolactin ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Growth Factor I

ABSTRACT Treatment of neonatal rats on days 2–5 with antibodies against rat GH (rGH) markedly reduced body weight gain and serum concentrations of insulin-like growth factor-I for 6–8 weeks in both females and males, after which weight gain normalized without evidence of catch-up growth. There were no significant effects on serum prolactin, tri-iodothyronine or corticosterone. Testis and ovarian weights were reduced, although only in proportion to body size. In females, but not males, the treated rats, though lighter, had increased fat deposition in the parametrial depot. Pituitary weight was considerably reduced over 100 days later, as was the pituitary content of GH, but not prolactin. The response to GH-releasing factor of both male and female rats was also greatly reduced at this time. Taken together with the fact that these rGH antibodies can bind directly to somatotrophs, we propose that the long-term effects of the antibodies are induced by specific somatotroph destruction. Journal of Endocrinology (1990) 124, 381–386

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