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PubMedDate not supplied

Digestive and metabolic adaptations of ruminants to undernutrition, and consequences on reproduction.

In response to undernutrition, short- (days) and medium-term (weeks) adaptations are more pronounced for splanchnic organs than for other tissues. For the latter, the long-term response involves a sequential mobilization (fat > muscle > bone) with relative priorities differing among anatomical sites. Among chemical components, the body lipids are extensively used (up to 80%) in underfed animals, while the range of protein utilization is limited (up to 15-20%). The decrease in energy expenditure during undernutrition is mostly due to a short- and medium-term decrease in feeding activity, and in the mass and activity of splanchnic tissues. In the long-term, energy expenditure and tissue masses decrease concomitantly, but there does not appear to be a significant decrease in expenditure per unit tissue weight. Nitrogen losses decrease in response to decline in nitrogen fluxes and also due to sparing by renal activities and sometimes by urea recycling. However, ruminants do not seem to be able to compensate for a low level of intake (below maintenance) by an increase in digestive efficiency. Numerous hormones (insulin, growth hormone, insulin-like growth factor I, catecholamines, thyroid hormones, cortisol, leptin, etc.) are involved in the changes during undernutrition of nutrient fluxes between tissues, either through control of synthesis and/or degradation in peripheral tissues (adipose tissue and muscle), or through hepatic conversions of substrates (gluconeogenesis, ureagenesis and ketogenesis), in order to maintain the constancy of the internal environment (homeostasis) and/or to sustain productive functions (teleophoresis). However, reproductive process may be blocked in underfed animals.

Adaptation, Physiological↗
PubMed2000

Suppression of preadipocyte differentiation and promotion of adipocyte death by HIV protease inhibitors.

Many human immunodeficiency virus (HIV)-infected patients taking combination antiretroviral therapy that includes HIV protease inhibitors experience atrophy of peripheral subcutaneous adipose tissue. We investigated the effects of HIV protease inhibitors on adipogenesis and adipocyte survival using the 3T3-L1 preadipocyte cell line. Several HIV protease inhibitors were found either to inhibit preadipocyte differentiation or to promote adipocyte cell death. One protease inhibitor, nelfinavir, elicited both of these effects strongly. When induced to differentiate in the presence of nelfinavir, 3T3-L1 preadipocytes failed to accumulate cytoplasmic triacylglycerol and failed to express normal levels of the adipogenic transcription factors CCAAT/enhancer-binding protein alpha and peroxisome proliferator-activated receptor gamma. The level of the proteolytically processed, active 68-kDa form of sterol regulatory element-binding protein-1, a transcription factor known to promote lipogenic gene expression, also was reduced markedly in nelfinavir-treated cells, whereas the level of the 125-kDa precursor form of this protein was unaffected. The inhibitory effect of nelfinavir occurred subsequent to critical early events in preadipocyte differentiation, expression of CCAAT/enhancer-binding protein beta and completion of the mitotic clonal expansion phase, because these events were unaffected by nelfinavir treatment. In addition, nelfinavir treatment of fully differentiated 3T3-L1 adipocytes resulted in DNA strand cleavage and severe loss of cell viability. In contrast, cell proliferation and viability of preadipocytes were unaffected by nelfinavir treatment. Thus, molecular or cellular changes that occur during acquisition of the adipocyte phenotype promote susceptibility to nelfinavir-induced cell death. When considered together, these results suggest that nelfinavir may promote adipose tissue atrophy by compromising adipocyte viability and preventing replacement of lost adipocytes by inhibiting preadipocyte differentiation.

3T3 Cells↗
PubMed1999

Metabolic abnormalities and body fat redistribution in HIV-1 infected patients: the lipodystrophy syndrome.

A unique and unexpected syndrome consisting of metabolic abnormalities (hyperlipidaemia and insulin resistance) and body fat redistribution (central adiposity and peripheral fat wasting) has been reported with increasing frequency in HIV-1 infected patients, most of whom are receiving highly active antiretroviral therapies including HIV-1 protease inhibitors. This article reviews the clinical and laboratory characteristics, the pathogenesis, and the management of this syndrome.

Journal Article↗
PubMed1996

Acute effects of caffeine ingestion at rest in humans with impaired epinephrine responses.

Caffeine ingestion has been demonstrated to increase circulating epinephrine (Epi) and norepinephrine (NE), elevate free fatty acids (FFAs), and alter heart rate, blood pressure (BP), and ventilation in humans. Whether these physiological responses are a result of caffeine acting through direct stimulation of specific tissues via adenosine receptors or secondary to Epi increases is not known. In the present experiment, six tetraplegics (level of spinal cord lesions C4-C6) were tested at rest for 3 h to investigate the effects of 6 mg/kg caffeine in capsule form on subjects with impaired Epi responses. Ventilatory, cardiovascular, metabolic, and hormonal data were collected every 15-20 min after caffeine ingestion. There were no significant (P > 0.05) increases in plasma Epi after caffeine ingestion [0.19 +/- 0.04 (SE) nM (preingestion); 0.20 +/- 0.04 nM (80 min postingestion)] or in plasma NE [0.53 +/- 0.16 nM (preingestion); 0.49 +/- 0.09 nM (80 min postingestion; P > 0.05)]. However, significant increases were found in serum FFAs [0.53 +/- 0.08 nM (preingestion); 1.03 +/- 0.20 mM (40 min postingestion; P < 0.05] and in glycerol. These concentrations remained elevated throughout the experiment. BP increased in the first hour postingestion. These data demonstrate that caffeine in physiological doses directly stimulates specific tissues, i.e., adipose and peripheral vascular tissue, and these effects are not secondary to increases in Epi after caffeine ingestion.

Adult↗
PubMed2004

Central administration of ghrelin and agouti-related protein (83-132) increases food intake and decreases spontaneous locomotor activity in rats.

Ghrelin was recently identified as an endogenous ligand of the GH secretagogue receptor. The novel peptide hormone is produced by gastric A-like cells, and circulating levels rise before feeding, suggestive of ghrelin as an endogenous hunger factor. ghrelin stimulates food intake and promotes adiposity after peripheral or central administration, likely by activating hypothalamic neurons expressing the orexigenic neuropeptides neuropeptide Y (NPY) and agouti-related protein (AGRP). To examine whether ghrelin-induced feeding resembles NPY and AGRP [AGRP fragment (83-132)] induced orexia, we compared the short- and long-term orexigenic capacity of the three peptides. A single intracerebroventricular injection of ghrelin (0.2, 1.0, and 5.0 microg) increased food intake in a dose-dependent manner. A prolonged and uncompensated increase in feeding was seen after the highest dose of ghrelin. The prolonged effects on feeding (+72 h) closely resembled those of AGRP (83-132) but not NPY. Surprisingly, ghrelin injections reduced overall locomotor activity by 20% during the first 24-h observation period. AGRP (83-132) had similar effects on locomotor behavior, whereas NPY had no effect. In summary, ghrelin causes long-term increases of food intake and, like AGRP, plays a previously unknown role as a suppressor of spontaneous physical activity. Expanding the current model of food intake control to include mechanisms regulating physical activity may promote our understanding of two major etiological factors causing obesity.

Agouti-Related Protein↗
PubMed2005

Insulin resistance in the HIV-infected population: the potential role of mitochondrial dysfunction.

Insulin resistance is accepted as the underlying fundamental defect that predates and ultimately leads to the development of type 2 (adult onset) diabetes mellitus in the general non-human immunodeficiency virus (HIV)-infected population. Insulin resistance is also a major component of the metabolic syndrome that, in association with other factors such as hypertension, hypercholesterolemia, and central obesity, defines a pre-diabetic atherogenic state that leads to adverse cardiovascular events. Growing evidence now suggests that mitochondrial dysfunction in skeletal muscle may be the mechanism whereby insulin resistance is induced. The prevalence of insulin resistance, glucose intolerance, and diabetes in the HIV-infected population has dramatically increased following the common use of highly active antiretroviral therapy (HAART). The development of insulin resistance in the HIV-infected population is likely to be multifactorial reflecting genetic predisposition, direct and indirect effects of both the protease inhibitor (PI) and nucleoside reverse transcriptase inhibitor (NRTI) class of antiretroviral therapy, and a possible contribution from chronic inflammatory changes induced by HIV. Indirect effects of antiretroviral therapy on insulin resistance may be mediated through both the visceral adiposity and peripheral fat depletion components of lipodystrophy as well as through fatty infiltration in liver and muscle. Based on current knowledge, mitochondrial dysfunction can be hypothesized to play a key role in each of these components.

Acquired Immunodeficiency Syndrome↗
PubMed2005

[Progress of study on placenta mesenchymal stem cells--review].

Recently mesenchymal stem cells have been successfully obtained from various sources of human body, including bone marrow, compact bone, peripheral blood, adipose tissue, cord blood, amniotic fluid and other fetal tissues. Placenta, as a temporary organ keeping substance exchange between mother and fetus, consisted of decidua basalis and chorion frondosum, which derived from cytotrophoblast and extraembryonic mesoderm, thus involved both primary embryonic cells and adult stem cells. As a castoff after parturition, along with the ease of accessibility, lack of ethical concerns, placenta may be an attractive source of mesenchymal stem/progenitor cells for basic and clinical application. Therefore, the origin, isolation, characteristics and potential uses in future therapy are mainly reviewed in this paper.

Cell Differentiation↗
PubMed2006

Heart involvement in lamin A/C related diseases.

The LMNA gene encodes lamins A and C, components of the nuclear envelope. Its mutations cause a wide range of diseases named laminopathies involving either specific tissues in isolated fashion (cardiac and skeletal muscles, peripheral nerve, adipose tissue) or several tissues in a generalized way (premature ageing syndromes and related disorders). The striated muscle laminopathies include a variety of well clinically characterized disorders where cardiac muscle involvement represents the common feature that coexists with or without skeletal muscle disease. The cardiac disease of LMNA mutated patients is classically defined by conduction system and rhythm disturbances occurring early in the course of the disease, followed by dilated cardiomyopathy and heart failure. These features are life threatening and often responsible of cardiac sudden death. When associated, the skeletal muscle involvement is characterized by muscle weakness and wasting of variable topography with or without early joint contractures and spinal rigidity. Specific management of the cardiac disease to includes antiarrhythmic drugs, cardiac devices such as implantable cardioverter for primary and secondary prevention of sudden death, and heart transplantation at the end stage of heart failure. A large number of LMNA mutations leading to striated muscle laminopathies have been reported without so far any clear and definite phenotype/genotype relation. Finally, among the diverse hypotheses for pathomechanisms of LMNA mutations, the structural hypothesis suggesting a defective role of lamins A/C in maintaining the structural integrity of the nuclear envelope in striated muscles under constant mechanical stress is highly attractive to link the LMNA mutations and the cardiac disease.

Heart Conduction System↗
PubMed2006

Mesenchymal stem cells: characteristics and clinical applications.

Mesenchymal stem cells (MSCs) are bone marrow populating cells, different from hematopoietic stem cells, which possess an extensive proliferative potential and ability to differentiate into various cell types, including: osteocytes, adipocytes, chondrocytes, myocytes, cardiomyocytes and neurons. MSCs play a key role in the maintenance of bone marrow homeostasis and regulate the maturation of both hematopoietic and non-hematopoietic cells. The cells are characterized by the expression of numerous surface antigens, but none of them appears to be exclusively expressed on MSCs. Apart from bone marrow, MSCs are located in other tissues, like: adipose tissue, peripheral blood, cord blood, liver and fetal tissues. MSCs have been shown to be powerful tools in gene therapies, and can be effectively transduced with viral vectors containing a therapeutic gene, as well as with cDNA for specific proteins, expression of which is desired in a patient. Due to such characteristics, the number of clinical trials based on the use of MSCs increase. These cells have been successfully employed in graft versus host disease (GvHD) treatment, heart regeneration after infarct, cartilage and bone repair, skin wounds healing, neuronal regeneration and many others. Of special importance is their use in the treatment of osteogenesis imperfecta (OI), which appeared to be the only reasonable therapeutic strategy. MSCs seem to represent a future powerful tool in regenerative medicine, therefore they are particularly important in medical research.

Antigens, Differentiation↗
PubMed1991

[Protective effect of intrastriatal grafts in an experimental model of Huntington's disease. Behavioral and morphological correlation].

The intrastriatal injection of the excitotoxin quinolinic acid (Q.A.) in rats produces neuroanatomical and neurochemical changes mimicking those appearing in the striatum in Huntington's disease (H.D.). Although its cause is unknown, it has been hypothesized that the neurodegenerative changes seen in H.D. may result from the action of an endogenous toxin. Therefore, the development of new strategies for limiting or preventing Q.A.-or other neurotoxic-induced degeneration may be of therapeutic interest for neurodegenerative disorders. Accordingly, we tested the ability of various tissue transplants to protect the rat striatum against a subsequent Q.A. insult. Using a "unilateral model", i.e. unilateral intrastriatal grafts followed by an ipsilateral intrastriatal injection of Q.A., we were able to quantify a behavioral protective effect of the grafts in recording the apomorphine-induced rotational behavior that normally appears after the striatal Q.A.-induced lesion. Our results show that one of the tested tissue, fetal striatum, protects the recipients against the lesioned-induced rotational behavior that appeared in non-grafted lesioned animals. The other grafted tissues (adrenal medulla, peripheral nerve, adipose tissue) seemed to provide a less dramatic protection than fetal striatum; however, this difference did not reach significance. Quantification of the striatal neuronal loss showed that the behavioral protection is significantly correlated with a better neuronal survival in the grafted animals. These results suggest that intracerebral grafts can protect the host brain against a toxin-induced damage, like the one resulting from Q.A. intrastriatal injection. Though fetal striatal grafts seem to exert an optimal protection, this protective effect may at least partially result from a host-mediated response to the transplantation procedure. The mechanism underlying this protective effect is unclear, but the present data suggest that it might be related to a transplantation-induced astroglial reaction resulting in an increased neuronotrophic activity that could protect against the toxic effect of Q.A. The results of this study also support the concept that the effect of transplantations could occur through processes other than a direct restoration of deficient transmitters or a reconstruction of damaged pathways. Further characterization of the factors implicated in the present paradigm might conceivably open avenues for possible therapeutic preventive interventions in neurodegenerative disorders.

Animals↗
PubMed1981

Alteration of the intracellular calcium pool of adipose tissue in spontaneously hypertensive rats. No effect of peripheral immunosympathectomy.

The intracellular calcium pool of adipose tissue was estimated by studying the kinetics of 45Ca efflux from the tissue of 9-week old spontaneously hypertensive (SHR) and normotensive Kyoto-Wistar (NKWR) rats subjected to peripheral immunosympathectomy (nerve growth factor antiserum treatment of newborn rats) and in intact (sham-treated) animals of both strains. The development of hypertension in SHR was prevented by immunosympathectomy, however, both groups, SHR-intact and immunosympathectomized rats showed an increase in the intracellular calcium content of adipocytes. These results indicate that the alteration of the membrane control over intracellular calcium distribution in adipose tissue of SHR cannot be attributed to an enhanced activity of the sympathetic nervous system.

Adipose Tissue↗
PubMed2005

Rhythmic messenger ribonucleic acid expression of clock genes and adipocytokines in mouse visceral adipose tissue.

Various peripheral tissues show circadian rhythmicity, which is generated at the cellular level by their own core oscillators that are composed of transcriptional/translational feedback loops involving a set of clock genes. Although the circulating levels of some adipocytokines, i.e. bioactive substances secreted by adipocytes, are on a 24-h rhythmic cycle, it remains to be elucidated whether the clock gene system works in adipose tissue. To address this issue, we investigated the daily mRNA expression profiles of the clock genes and adipocytokines in mouse perigonadal adipose tissues. In C57BL/6J mice, all transcript levels of the clock genes (Bmal1, Per1, Per2, Cry1, Cry2, and Dbp) and adipocytokines (adiponectin, resistin, and visfatin) clearly showed 24-h rhythms. On the other hand, the rhythmic expression of these genes was mildly attenuated in obese KK mice and greatly attenuated in more obese, diabetic KK-A(y) mice. Obese diabetes also diminished the rhythmic expression of the clock genes in the liver. Interestingly, a 2-wk treatment of KK and KK-A(y) mice with pioglitazone impaired the 24-h rhythmicity of the mRNA expression of the clock genes and adipocytokines despite the antidiabetic effect of the drug. In contrast, pioglitazone improved the attenuated rhythmicity in the liver. These findings suggest that the intracellular clock gene system acts in visceral adipose tissues as well as liver and is influenced by the conditions of obesity/type 2 diabetes and pioglitazone treatment.

Adipocytes↗
PubMed2002

Leptin--from a signal of adiposity to a hormonal mediator in peripheral tissues.

The biology of leptin has been studied most extensively in the central nervous system for the regulation of food intake and energy balance. In recent years, a growing number of publications have reported several activities of this adipose-secreted protein in different organs. These effects appear to be independent of the regulation of food intake or at least not directly correlated to it, but rather related to the hormonal regulation of these particular tissues. Thus leptin is now also considered to be a hormonal factor that informs several hormonal circuits and biological peripheral functions of the nutrition status of the organism. Different systems are involved in leptin activity, such as the pituitary, male and female reproductive organs, the mammary gland, the immune system, the gut, the kidney and the lung. Functional leptin receptors and/or leptin protein have been shown to be expressed in these tissues. Furthermore, interesting interactions have been reported with classical hormones involved in the regulation of activities in such organs. These observations give more detailed evidence of the relationship between nutrition and tissue differentiation in peripheral sites, possibly mediated by classical hormonal circuits. This work aims to review the most important functional findings on leptin's effects in these peripheral sites, and potential future studies are suggested, based on currently available data.

Adipose Tissue↗
PubMed1982

Role of human adipose tissue in the production and metabolism of steroid hormones.

Radioimmunological methods have been employed for the simultaneous determination of dehydroepiandrosterone, androstenedione, testosterone, oestrogens (oestradiol + oestrone), progesterone, 17 alpha-hydroxyprogesterone and cortisol in human adipose tissue and peripheral blood to compare the hormone pool of adipose tissue with that in the general circulation. Extremely high steroid concentrations in the adipose tissue and hormone pool in the fat of obese subjects were observed. For adipose tissue/serum steroid ratios, the highest values were obtained for dehydroepiandrosterone and the lowest ones for cortisol. A preliminary study showed a great accumulation of steroids in adjacent adipose tissue of breast tumors. Striking differences were observed in the adipose tissue steroid concentrations between benign and malignant mammary tumors. The present findings revealed that blood hormone determinations may be insufficient to consider the steroid hormone availability in various endocrinopathies or steroid responsive tumors, especially when the endocrine state of extremely obese subjects is observed.

17-alpha-Hydroxyprogesterone↗
PubMed1999

Body fat distribution and hemodynamic stress responses in premenopausal obese women: a preliminary study.

To examine the relationship between body fat distribution and hemodynamic stress responses, cardiovascular responses to a speech task and a forehead cold pressor task were evaluated with 24 premenopausal women classified a priori as either centrally or peripherally obese. Results showed that women with central adiposity exhibited greater stress-related increases in diastolic blood pressure and total peripheral resistance, whereas women with peripheral adiposity exhibited greater stress-related increases in cardiac output. Depression, self-consciousness, hostility, and mood scores did not explain significant variance in the stress response differences between regional adiposity groups. The findings suggest that central adiposity may increase the risk of cardiovascular disease in women at least in part by enhancing vascular responses to stress.

Adipose Tissue↗
PubMed2004

c-Cbl-deficient mice have reduced adiposity, higher energy expenditure, and improved peripheral insulin action.

Casitas b-lineage lymphoma (c-Cbl) is an E3 ubiquitin ligase that has an important role in regulating the degradation of cell surface receptors. In the present study we have examined the role of c-Cbl in whole-body energy homeostasis. c-Cbl-/- mice exhibited a profound increase in whole-body energy expenditure as determined by increased core temperature and whole-body oxygen consumption. As a consequence, these mice displayed a decrease in adiposity, primarily due to a reduction in cell size despite an increase in food intake. These changes were accompanied by a significant increase in activity (2- to 3-fold). In addition, c-Cbl-/- mice displayed a marked improvement in whole-body insulin action, primarily due to changes in muscle metabolism. We observed increased protein levels of the insulin receptor (4-fold) and uncoupling protein-3 (2-fold) in skeletal muscle and a significant increase in the phosphorylation of AMP-activated protein kinase and acetyl-CoA carboxylase. These findings suggest that c-Cbl plays an integral role in whole-body fuel homeostasis by regulating whole-body energy expenditure and insulin action.

AMP-Activated Protein Kinases↗
PubMed1983

Hibernoma: distinctive light and electron microscopic features and relationship to brown adipose tissue.

Four hibernomas and samples of developing human brown and white adipose tissue were observed. Distinctive features of hibernomas were 1) lobules of closely apposed large polygonal cells and capillaries; 2) three principal cell types (granular eosinophilic, multivacuolated, and univacuolated) varying in prominence from case to case; 3) investment of each tumor cell by basal lamina; 4) an inverse relationship between lipid droplet size and the number of mitochondria per unit of cytoplasm; 5) pleomorphic mitochondria with dense matrixes or large, round mitochondria with transverse lamellar cristae; 6) undulating plasmalemmal invaginations; 7) micropinocytotic vesicles; 8) periodic short plasmalemmal densities; and 9) a conspicuous lack of cytoplasmic membrane systems. The frequent association of micropinocytotic vesicles and undulating plasmalemmal invaginations in proximity to capillaries strongly suggests that the invaginations represent a localized cell membrane adaptation for efficient endocytosis. In human fetal brown adipose tissue, which is first recognizable in fetuses of 21 weeks' gestational age, the most characteristic cell was the polygonal multivacuolated cell. Univacuolated cells were present in brown adipose tissue of older fetuses, and in infants and adults entire lobules containing univacuolated cells coexisted with lobules of multivacuolated cells and granular eosinophilic cells. The ultrastructure of human brown adipose tissue resembled that of hibernomas and was similar to previously described features of this tissue in animals. Developing white adipose tissue differed from brown adipose tissue by its loose plexiform arrangement of capillaries and spindle-shaped cells in less circumscribed lobules and by the absence of polygonal multivacuolated cells. The authors did not identify centripetal lobular maturation in white adipose tissue, but peripheral growth "caps" were a common finding in maturing brown adipose tissue. They consider brown adipose tissue to be a special form of adipose tissue, the variable cytologic composition of which is reflected in the histologic spectrum of hibernomas.

Adipose Tissue, Brown↗
PubMed1992

Fat distribution: its physiological significance, health implications, and its adaptation to exercise training.

Recently, fat distribution has become of clinical interest in assessing one's risk for coronary heart disease (CHD). Investigations have shown stronger relationships between abdominal, or central adiposity, and various well known risk factors for CHD, than peripheral and/or total adiposity. The simple waist-to-hip ratio, shown to be a valid index of such fat distribution, should be considered for use by professionals in military medicine in assessing one's risk for relevant diseases. Consideration must also be made of the role of exercise as an intervention in improving one's fat distribution profile.

Adipose Tissue↗