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S Lemieux

Publications and source records attributed to S Lemieux.

At least 55 records · Page 3Linked to original sources
PubMed1997

Genetic susceptibility to visceral obesity and related clinical implications.

This paper reviews evidence supporting the notion that genetic factors may have an influence on the determination of body fat distribution, particularly emphasizing the genetic susceptibility of visceral adipose tissue (AT) accumulation. The potential contribution of genetic susceptibility to the development of metabolic alterations in visceral obese individuals will also be reviewed. The contribution of genetic factors to the variation in body fat distribution is supported by studies in which racial differences in body fat distribution were reported. These ethnic differences suggest that body fat distribution may be influenced by some components of the genetic background which are shared among individuals of a given race. Furthermore, the familial aggregation and the resemblance between monozygotic twins that have been observed for anthropometric measurements of body fat distribution and for visceral AT accumulation measured by computed tomography, also suggest that genetic factors are involved in the determination of body fat distribution. Genetic susceptibility may also influence the relationship between visceral AT accumulation and the development of metabolic alterations. In this regard, it has been reported that the polymorphism of some genes (for example, the apolipoprotein (apo) E, apo B100 and lipoprotein lipase genes) is altering the relationship between visceral obesity and plasma lipoprotein-lipid levels. In conclusion, results presented in this paper suggest that genetic factors seem to have a significant influence on the propensity to accumulate AT in the visceral depot and that genetic factors also seem to affect the associations commonly reported between visceral obesity and the development of metabolic alterations.

Adult↗
PubMed1997

The NK2.1 receptor is encoded by Ly-49C and its expression is regulated by MHC class I alleles.

A dual receptor system composed of activation and inhibitory receptors apparently controls NK cell-mediated lysis. In the C57BL/6 mouse, the NK1.1 molecule acts as an activation receptor whereas Ly-49A, C and G2 can inhibit NK cell lysis of target cells expressing specific MHC class I molecules. We previously reported that NK2.1 is an activation receptor sharing structural properties with members of the NKR-P1 and Ly-49 receptor families. In this study, we have shown that NK2.1 is encoded by the previously described Ly-49C gene. We also found that the expression level of NK2.1/Ly-49C is modulated by H-2-dependent factors and that this regulation differs from that previously described for Ly-49A. Flow cytometry analyses of NK-enriched spleen cells from MHC congenic strains on C57BL/10 and BALB/c backgrounds indeed revealed that the level of NK2.1/Ly-49C expression, but not the number of positive cells, is low in strains expressing H-2b and H-2k haplotypes as compared to H-2d mice. Similar analyses of splenic NK cells from two series of congenic and congenic recombinant strains on the C57BL/10 background indicate that the main regulatory element(s) are most likely the H-2Kb and H-2Dk alleles. Together with our and others previous observations, these results identify the NK2.1/Ly-49C antigen as a receptor for MHC class I molecules whose expression is regulated by host MHC genes.

Alleles↗
PubMed1997

Allorecognition by murine natural killer cells: lysis of T-lymphoblasts and rejection of bone-marrow grafts.

Natural killer (NK) cells of inbred mice reject allogeneic bone-marrow cells, and NK cells of F1 hybrid mice can reject parental bone-marrow cells (hybrid resistance). In some cases these patterns of rejection can be mimicked in vitro by utilizing IL-2 cultured NK effector cells and allogeneic or parental T-lymphoblasts as target cells. Lysis of allogeneic and parental targets in vitro can be explained on the basis of the missing self hypothesis. Subsets of NK cells that bear non-overlapping MHC class I inhibitory receptors belonging to the Ly49 family lyse allogeneic targets because they do not express self class I molecules of the NK cell donor. Parental strain targets are lysed because they do not express all of the self class I antigens of the F1 hybrid, and hence fail to deliver inhibitory signals to all subsets of F1 NK cells. The expression of Ly49 receptors on NK cells is regulated by host MHC to ensure maximal sensitivity to alterations in self class I molecules and to prevent autoreactivity. In many instances, however, the rejection of allogeneic bone marrow cells in vivo cannot be readily explained by the missing self hypothesis. In these instances, it appears that rejection is initiated by class I MHC receptors on NK cells that recognize allogeneic class I molecules as non-self, and activate rather than inhibit NK cell function.

Animals↗
PubMed1997

Chronic exogenous insulin and chronic carbohydrate supplementation increase de novo VLDL triglyceride fatty acid production in rats.

We have investigated hepatic de novo lipogenesis and the ratio of apoB-48/apoB-100 during chronic carbohydrate supplementation with or without administration of exogenous insulin in rats. Two groups received chronic (2 weeks) carbohydrate supplementation either as 10% glucose or 10% fructose (wt/v) in their drinking water. Two other groups received exogenous insulin chronically, in addition to the monosaccharides above. The insulin was given for 2 weeks as daily human ultralente insulin injections in increasing doses up to 6 units per day. A fifth group of rats (normal control) received only chow and water. The fractional synthetic rate (FSR), the fraction of very low density lipoprotein triglyceride (VLDL-TG) palmitate that was newly made during an 8-h infusion with sodium [1-13C]acetate, was evaluated. The glucose and fructose groups had a 4-fold (0.60%/h) and 7.5-fold (1.13%/h) increase in FSR from baseline, respectively, compared to chow-fed controls (0.15%/h). Chronic exogenous insulin administration resulted in a 11.5 (1.73%/h) and 11.0 (1.65%/h)-fold increase over baseline in the synthesis of newly made VLDL-TG palmitate in the glucose and fructose groups, respectively. The ratio of apoB-48/apoB-100, i.e. apoB-48 enrichment, in VLDL was positively correlated with insulin levels (r = 0.41, P < 0.01) and with FSR (r = 0.39, P < 0.01). The present study shows that carbohydrate supplementation significantly increases the FSR of newly made VLDL-TG palmitate and that this increase is further augmented by chronic hyperinsulinemia.

Acetates↗
PubMed1996

Heterogeneity among Ly-49C natural killer (NK) cells: characterization of highly related receptors with differing functions and expression patterns.

Ly-49C is a member of the polymorphic family of murine NK cell inhibitory receptors. The 5E6 antibody that defines a subset of NK cells responsible for the rejection of parental H-2d bone marrow by F1 mice has been shown previously to react with Ly-49C. Here, the 5E6 antibody was found to detect two Ly-49C-related molecules in B6 mice. Two cDNA clones were isolated from B6 NK cells, one identical to previously reported Ly-49CB6 and the other a novel cDNA. The deduced amino acid sequence of the latter differs from that of Ly-49CBALB at only 4 residues, whereas the previously reported Ly-49CB6 differs at 22 residues. Flow cytometric analyses of COS cells transfected with the two cDNAs showed that the 5E6 antibody binds to both Ly-49 molecules, while another anti-Ly-49C antibody, 4LO3311, binds to the newly described Ly-49C but not the previously reported Ly-49CB6. Two-color flow cytometric analysis detected 5E6+4LO3311- as well as 5E6+4LO3311+ subsets of NK cells from B6, but not BALB/c, mice. The level of Ly-49C expression on B6 NK cells detected by the 4LO3311 antibody was substantially lower than that on BALB/c NK cells. Binding specificity of the novel Ly-49CB6 was indistinguishable from that of Ly-49CBALB, whereas no binding was detectable with previously reported Ly-49CB6. These results demonstrate that the newly described Ly-49CB6, not the previously reported Ly-49CB6, is the probable B6 allelic form of Ly-49C. The previously reported Ly-49CB6 must be encoded by a separate gene and should be renamed Ly-49I. The implication of these results with respect to the role of Ly-49C in hybrid resistance is discussed.

Amino Acid Sequence↗
PubMed1996

Genetic control of anti-idiotypic vaccination against coronavirus infection.

The idiotypic network can be experimentally altered to induce protective immune responses against microbial pathogens. Both internal image and noninternal image anti-idiotypic (anti-Id) antibodies have been shown to trigger antigen (Ag)-specific immune responses. Therefore, mechanisms of anti-Id vaccination appear to go beyond structural mimicry of Ag, but remain undefined. Using the neurotropic murine coronavirus animal model, we have previously shown that a polyclonal noninternal image anti-Id (Ab2) could vaccinate BALB/c mice. To characterize its mode of action, we have examined the immune modulating capability of this Ab2 in vivo in strains of mice with different H-2 haplotypes. Even though only internal image anti-Id are expected to induce non-genetically restricted immunity, this noninternal image Ab2 induced protective immunity in four of eight genetically different strains of mice susceptible to coronavirus infection. These were BALB/c (H-2d), DBA/2 (H-2d), DBA/1 (H-2q), and SWR (H-2q) mice. Protection was generally correlated with the induction of specific antiviral Ab (Ab3) that showed biological properties, such as virus neutralization in vitro, similar to the initial Ab1. To evaluate the genetic implication of the H-2 haplotypes in protection, congenic mice were also tested. Vaccination profiles suggest that cooperation between background gene(s) of the BALB/c mouse with H-2d and H-2q loci is necessary for an optimal protective immune response, although the main genetic element(s) regulating the antiviral response to Ab2 inoculation appeared to be located outside the major histocompatibility complex. These results are consistent with the ability of Ab2 to induce protective antiviral antibodies in genetically different animals by biological mimicry.

Animals↗
PubMed1996

Familial aggregation of abdominal visceral fat level: results from the Quebec family study.

The purpose of this study was to investigate the importance of familial aggregation in abdominal visceral fat (AVF) level as assessed by computed tomography (CT). Four measures of abdominal adipose tissue, obtained from an abdominal scan between the fourth and fifth Lumbar vertebrae (L4-L5) taken in 366 adult subjects from 100 French-Canadian nuclear families, were considered in this study. Total abdominal fat, AVF, subcutaneous abdominal fat, obtained by computing the difference between total and AVF tissue areas, and the visceral to total abdominal fat ratio were measured. Spouses, parent-offspring, and sibling correlations were computed by maximum likelihood methods after adjustment of the four phenotypes for age and for age and total fat mass (FM) derived from underwater weighing. Significant familial aggregation was found for all phenotypes, whether adjusted or not for body FM. However, after adjustment of data for body FM, in addition to age, all spouse correlations became nonsignificant, suggesting that the familial aggregation of abdominal fat is primarily genetic. Heritability estimates reached 42% and 56% for subcutaneous fat and AVF, respectively. These results suggest that genetic factors are major determinants of the familial aggregation observed in the amount of abdominal fat, irrespective of total body fat content, and that AVF seems more influenced by genetic factors than abdominal subcutaneous adipose tissue. These findings imply that some individuals are more at risk than others to exhibit the various metabolic complications associated with upper-body obesity because of their inherited tendency to store abdominal fat in the visceral depot rather than in the subcutaneous depot.

Abdomen↗
PubMed1996

A single threshold value of waist girth identifies normal-weight and overweight subjects with excess visceral adipose tissue.

Our objective was to determine threshold values of waist girth, waist-to-hip ratio (WHR), and sagittal diameter corresponding to an accumulation of visceral adipose tissue of 130 cm2 and to verify whether these threshold values could be influenced by sex, age, menopausal status, and the degree of obesity. From the regression equations computed in the total sample of 213 men [aged (mean+/- SD) 37.8 +/- 12.2 y] and 190 women (aged 37.3 +/- 12.1 y), a waist girth of approximately 95 cm in both sexes, WHR values of 0.94 in men and of 0.88 in women, and sagittal diameters of 22.8 cm in men and 25.2 cm in women corresponded to a visceral adipose tissue area of 130 cm2. In both sexes, threshold values of waist girth corresponding to critical amounts of visceral adipose tissue were generally lower in subjects who were > or = 40 y old (approximately 90 cm) than in younger individuals (approximately 100 cm). Similar differences were found for WHR and sagittal diameter threshold values. Finally, threshold values of waist girth corresponding to critical amounts of visceral adipose tissue were essentially similar in normal-weight and overweight men and women, whereas threshold values of WHR were in general higher in normal-weight than in overweight subjects. In conclusion, our results suggest that the relations of anthropometric variables to visceral adipose tissue accumulation are age-specific. However, waist girth is likely to be a more convenient anthropometric correlate of visceral adipose tissue than the WHR because threshold values of waist girth corresponding to critical amounts of visceral adipose tissue do not appear to be influenced by sex or by the degree of obesity.

Adipose Tissue↗
PubMed1996

Seven-year changes in body fat and visceral adipose tissue in women. Association with indexes of plasma glucose-insulin homeostasis.

OBJECTIVE: To study the associations between changes in body fatness, visceral adipose tissue (AT), and indexes of plasma glucose-insulin homeostasis over a 7-year follow-up period. RESEARCH DESIGN AND METHODS: A sample of 30 nondiabetic women aged 35.2 +/- 5.6 (SD) years at baseline was studied. RESULTS: Changes in visceral AT and in subcutaneous AT (measured by computed tomography) as well as changes in body fat mass (obtained by hydrostatic weighting) were significantly related to changes in fasting plasma insulin levels and in plasma insulin area measured after a 75-g oral glucose load (0.47 < or = r < or = 0.62; P < 0.01). Changes in visceral AT but not in body fat mass or in subcutaneous AT area were significantly associated with changes in plasma glucose area (r = 0.37; P < 0.05). When two subgroups of women with similar mean increases in body fat mass but with either small or large increases in visceral AT were compared, the subgroup with the largest gain in visceral AT showed the greatest deterioration in indexes of plasma glucose-insulin homeostasis. On the other hand, when two subgroups with similar mean increases in visceral AT but with different changes in body fat mass were compared, both subgroups showed similar changes in plasma glucose and insulin concentrations. CONCLUSIONS: Results of this 7-year follow-up study in women suggest that changes in indexes of plasma glucose-insulin homeostasis are significantly associated with changes in visceral AT, even after control for changes in body fat mass.

Adipose Tissue↗
PubMed1996

Major gene for abdominal visceral fat area in the Québec Family Study.

OBJECTIVES: The abdominal visceral fat depot is considered to be the most atherogenic, diabetogenic and hypertensiogenic fat depot of the human body. Although the amount of abdominal visceral fat is correlated with total body fat, there remain considerable inter-individual differences in visceral fat at any level of body fat content. No study has been reported to date on the contribution of genetic factors to the variability in abdominal visceral fat level. DESIGN: Abdominal visceral fat area was assessed by computerized tomography in 382 adult men and women from 100 families of the Québec Family Study. After adjustment for the effects of age and age plus total fat mass (assessed by underwater weighing), a major gene hypothesis for abdominal visceral fat area was investigated using segregation (POINTER) analyses. RESULTS: Segregation analysis of the age-adjusted variable indicated that variability in visceral fat area was accounted for by a major gene transmitted according to Mendelian expectations. Data support an autosomal recessive locus, associated with high levels of abdominal visceral fat, accounting for 51% of the phenotypic variance and affecting 10% of the sample. An additional 21% of the variance was due to multifactorial (polygenic and/or familial environment) sources. However, after adjusting for total fat mass, support for a major gene for abdominal visceral fat was less strong. CONCLUSIONS: These results suggest that the familial etiology of abdominal visceral fat level involves a major autosomal recessive locus. Given the critical role of abdominal visceral fat in the metabolic complications of obesity, it will now be important to identify the gene responsible for the high levels of abdominal visceral fat observed in some adults and to investigate whether this gene is the same as that which influences total body fat content.

Abdomen↗
PubMed1996

Anthropometric correlates to changes in visceral adipose tissue over 7 years in women.

OBJECTIVE: To investigate the association between either increases or decreases in visceral adipose tissue and changes in anthropometric indices in a group of 32 women studied over a 7-y period. SUBJECTS: 32 women aged 35.1 +/- 5.4 (SD) years at baseline. MEASUREMENTS: Waist and hip circumferences, body fat mass (hydrostatic weighing) and viscera adipose tissue (computed tomography) were measured at baseline and at follow-up. RESULTS: Waist girth, waist-to-hip ratio, sagittal diameter and visceral adipose tissue area were all significantly higher at follow-up than at baseline (p < 0.05). Changes in visceral adipose tissue area were strongly correlated to changes in waist girth, hip girth, sagittal diameter and body fat mass (0.80 < or = r < or = 0.91 p < 0.0001). However, the association between changes in waist-to-hip ratio and those in visceral adipose tissue area was of low magnitude (r = 0.35; p = 0.05). Partial correlation analyses showed that the association between changes in visceral adipose tissue area and changes in either waist girth (p < 0.01) or sagittal diameter (p < 0.0001) remained significant even after control for 7-y variation in total body fatness. CONCLUSION: Results of the present study suggest that changes in visceral adipose tissue accumulation that occur with age in women are better predicted by changes in waist girth or sagittal diameter than by changes in waist-to-hip ratio.

Adipose Tissue↗
PubMed1996

Associations between 12 year changes in body fatness and lipoprotein-lipid levels in men and women of the Québec Family Study.

OBJECTIVE: To investigate the associations between 12 year changes in body composition, subcutaneous fat distribution vs changes in plasma lipoprotein-lipid levels. DESIGN: 12 year prospective study. SUBJECTS: A sample of 95 women and 93 men of the Québec Family Study initially tested in 1980. MEASUREMENTS: Various body fatness variables as well as fasting plasma lipoprotein-lipid concentrations performed both in 1980 and 1992. RESULTS: In both 1980 and 1992, a high body fat mass and an elevated accumulation of subcutaneous trunk fat were associated with a significant deterioration in the plasma lipoprotein-lipid profile. Furthermore, correlation analysis performed on differences noted during the 12 years follow-up revealed significant associations between changes in body fat mass and in plasma cholesterol [r = 0.52, P < 0.0005] in women. In both men and women, an increased body fat mass was associated with an increased CHOL/HDL-cholesterol ratio [r = 0.37, P < 0.01 (men) and r = 0.54, P < 0.0005 (women)]. Correlations between changes in fat mass and plasma lipids were generally of higher magnitude in women than in men. Changes in subcutaneous trunk fat were associated with changes in plasma HDL-chol levels (r = -0.22, P < 0.05) in men whereas in women, changes in trunk adiposity were related to changes in both plasma CHOL (r = 0.25, P < 0.05) and TG (r = 0.32, P < 0.005) levels. CONCLUSION: These results support the notion that the increased adiposity observed among aging adult men and women is a significant component of the deterioration in the plasma lipoprotein-lipid profile noted over a 12 year follow-up period.

Adipose Tissue↗
PubMed1995

Cellular target of in vitro-induced suppressor cells derived from the spleen of Mycobacterium lepraemurium-infected mice and role of IFN-gamma in their development.

Unfractionated spleen cells from C3H mice infected a few weeks before with Mycobacterium lepraemurium developed a suppressor activity after overnight culture. This requires contact of plastic adherent cells with nonadherent cells distinct from T, B, or natural killer cells. The present study demonstrates that anti-interferon-gamma (IFN-gamma) monoclonal antibody and indomethacin totally abrogate the expression, although not the induction, of this activity. Furthermore, culture-induced suppressor cells selectively inhibit T lymphocyte proliferation, probably by altering the generation of interleukin-2 (IL-2) responsiveness through reduction of the affinity and density of high-affinity IL-2 receptors on activated cells. These and other previously determined properties of culture-induced suppressor cells, similar to those of adherent suppressor cells detected in freshly harvested spleen cells at a later stage of M. lepraemurium infection, suggest a common precursor. If so, the present observations should help in defining a strategy to prevent the impairment of cell-mediated immunity in infected mice.

Animals↗
PubMed1995

Do elevated levels of abdominal visceral adipose tissue contribute to age-related differences in plasma lipoprotein concentrations in men?

Age-related differences in body fat and more specifically in the accumulation of abdominal visceral adipose tissue were examined as a potential covariate for the alteration in the plasma lipoprotein profile found with aging. For that purpose, results from 79 young adults (aged 24.5 +/- 4.0 years) were compared to 61 middle-aged men (54.7 +/- 6.4 years). Younger men had significantly lower body fat mass and abdominal visceral adipose tissue area measured by computed tomography than middle-aged men (P < 0.0001). Plasma cholesterol, triglyceride, apolipoprotein (apo) B, low density lipoprotein (LDL)-cholesterol and LDL apo B levels, as well as the ratio of plasma cholesterol to high density lipoprotein (HDL)-cholesterol were all significantly lower in younger men as compared to middle-aged men (P < 0.0001). The comparison of younger men to middle-aged men with comparable levels of abdominal visceral fat and total body fat eliminated the age-related differences in plasma triglyceride and in the ratio of plasma cholesterol to HDL-cholesterol, whereas the difference in plasma apolipoprotein B levels, although still significant, was largely reduced. Age-related differences in plasma cholesterol and in LDL-cholesterol levels were still observed after this matching procedure and the differences between age-groups were essentially of similar magnitude than before pairing. In summary, these results suggest that the deterioration of plasma lipoprotein profile observed in middle-aged men as compared to young adult men is partly mediated by concomitant increases in total body fat and abdominal visceral adipose tissue. However, other factors related to the aging process appear to be involved, particularly for the age-related increase in plasma LDL-cholesterol.

Adipose Tissue↗
PubMed1995

Does lipoprotein or hepatic lipase activity explain the protective lipoprotein profile of premenopausal women?

Numerous studies have reported that women have a lipoprotein profile suggestive of a reduced risk of coronary heart disease (CHD). We have therefore tested whether the "protective" lipoprotein profile of women could be explained by differences in hepatic lipase (HL) or lipoprotein lipase (LPL) activities. In the present study, 14 non-obese healthy premenopausal women had higher plasma concentrations of high-density lipoprotein cholesterol (HDL-C), HDL2-C, HDL3-C, and HDL-apolipoprotein (apo) AI, and a higher ratio of HDL-C to low-density lipoprotein cholesterol (LDL-C) than 17 non-obese healthy men. Women also had lower plasma triglyceride (TG), HDL-TG, and apo B levels than men. Plasma postheparin LPL (PH-LPL) and HL activities showed no significant sex dimorphism, whereas abdominal and femoral adipose tissue (AT)-LPL activities were significantly higher in women (P < .005). In men, PH-LPL activity correlated significantly with plasma HDL2-C (r = .52, P < .05), LDL-C (r = -.47, P < .05), and apo B (r = -.56, P < .01) levels, as well as with the HDL-C/LDL-C ratio (r = .67, P < .005). No such relationships were found in women, with the exception of HL activity, which was negatively correlated with HDL-apo AI levels. In both genders, abdominal AT-LPL activity showed no significant association with plasma lipoprotein levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗
PubMed1995

Phenotypic characterization of two cell populations involved in the acquisition of suppressor activity by cultured spleen cells from Mycobacterium lepraemurium-infected mice.

The impairment of cellular immunity in mice infected with Mycobacterium lepraemurium was shown to correlate with the development of suppressor cells. We have previously reported that before suppressor activity is detectable in freshly harvested cell suspensions, suppressor cell precursors accumulate in the spleen of infected mice. Upon overnight culture in the presence of a regulatory cell subset, these precursor cells acquire the capacity to impair the concanavalin A (Con A)-induced proliferation of normal spleen cells. The purpose of this study was to determine the phenotype of the cells involved in this phenomenon. This was done by following the development of suppressor activity in spleen cell suspensions depleted of defined cell subsets of the adherent or the non-adherent cell fractions with selected MoAbs and immunomagnetic beads or by in vivo treatment. Our results indicate that the acquisition of suppressor activity requires the interaction of Ia+CD11b+Fc gamma R+IgG- asialo GM1- adherent cells with Thy1-CD4-CD8-IgG-Ia- asialo GM1-Fc gamma R+CD11b+ non-adherent cells. It is also shown that the development of suppressor activity is impaired by preventing cell-cell contact between these two cell subsets through coculture in 'Transwell chambers'. These observations support the conclusion that the in vitro acquisition of suppressor activity is a consequence of the maturation of suppressor cell precursors of the monocytic lineage induced by a receptor-ligand type interaction with a non-adherent cell subset that is clearly distinct from mature T, B and natural killer (NK) cells.

Animals↗
PubMed1995

Regional differences in adipose tissue lipolysis from lean and obese women: existence of postreceptor alterations.

Lipolysis studies were performed on isolated adipose cells obtained from two subcutaneous regions (abdominal and femoral) in 26 premenopausal women (16 obese and 10 lean subjects). Because obese adipocytes from both sites were significantly larger than lean fat cells, glycerol release measured by an ultrasensitive bioluminescent method was corrected for variation in cell surface area. Epinephrine induced antilipolysis at low concentrations and a net lipolytic response at higher doses, regardless of the subjects' fatness and the anatomic location of fat. However, the catecholamine and the selective alpha 2-adrenergic agonist, UK-14304, promoted a greater maximal antilipolytic response in both femoral and subcutaneous abdominal adipose cells from obese individuals that from lean individuals. Epinephrine- and UK-14304-induced maximal antilipolysis of femoral adipocytes was also positively associated with indicators of total adiposity. On the other hand, the maximal lipolytic responses to postadrenoceptor agents such as dibutyryl adenosine 3',5'-cyclic monophosphate, forskolin, and theophylline were lower in both adipose regions in obese than in lean women. Femoral fat cell lipolysis in the presence of these agents was negatively correlated with body fatness indexes. These results suggest that, in women covering a wide range of adiposity, variations in the lipolytic response of femoral fat cells to epinephrine may involve changes in the functional balance between alpha 2- and beta-adrenoceptors and also alterations located at different postreceptor levels.

Abdomen↗