Biomedical subjects
S Rössner
Publications and source records attributed to S Rössner.
Obesity in the elderly--a future matter of concern?
In most studies mean body weight increases with age up to about age 60 and then levels off, but information about the association between body weight and mortality at higher ages is sparse, since most studies published are cross-sectional, thus introducing a bias in selectivity. Some studies actually suggest a protective effect of overweight in the oldest age groups. Indices of visceral obesity may be better indicators of risk than body mass index (BMI) in these age groups. Not only actual weight, but also weight development over the last decades may predict outcome. Most clinical trials exclude older patients and little is known about benefits of diets or drugs inducing weight loss in these age groups. More information is available suggesting multiple benefits of physical activity. Mechanical complications of obesity, such as osteoarthritis and static respiratory complications seem to improve with weight loss even at higher ages. For health economic reasons it will become important to address treatment strategies in the elderly in the future, since they will constitute a large segment of the population. Recent studies suggest that bariatric surgery, previously considered contraindicated in obese patients above age 60 can be safely performed even in patients above age 70 and with the same benefits as for younger subjects.
Evidence for a major role of skeletal muscle lipolysis in the regulation of lipid oxidation during caloric restriction in vivo.
A lipolytic process in skeletal muscle has recently been demonstrated. However, the physiological importance of this process is unknown. We investigated the role of skeletal muscle lipolysis for lipid utilization during caloric restriction in eight obese women before and after 11 days of very low-calorie diet (VLCD) (2.2 MJ per day). Subjects were studied with indirect calorimetry and microdialysis of skeletal muscle and adipose tissue in order to analyze substrate utilization and glycerol (lipolysis index) in connection with a two-step euglycemic-hyperinsulinemic (12 and 80 mU/m(2). min) clamp. Local blood flow rates in the two tissues were determined with (133)Xe-clearance. Circulating free fatty acids and glycerol decreased to a similar extent during insulin infusion before and during VLCD, and there was a less marked insulin-induced reduction in lipid oxidation during VLCD. Adipose tissue glycerol release was hampered by insulin infusion to the same extent ( approximately 40%) before and during VLCD. Skeletal muscle glycerol release was not influenced by insulin before VLCD. However, during VLCD insulin caused a marked (fivefold) (P < 0.01) increase in skeletal muscle glycerol release. The effect was accompanied by a fourfold stimulation of skeletal muscle blood flow (P < 0.01). We propose that, during short-term caloric restriction, the reduced ability of insulin to inhibit lipids, despite a preserved antilipolytic effect of the hormone in adipose tissue, is caused by an augmented mobilization of fat from skeletal muscle, and that a physiological role of muscle lipolysis provides a local source of fatty acids.
[The Santa lives dangerously].
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Cutting edge: resistance to apoptosis and continuous proliferation of dendritic cells deficient for TNF receptor-1.
The individual roles of the two TNFRs on dendritic cells (DC) are poorly understood. Investigating bone marrow-derived DC from TNFR-deficient mice, we found that cultures from TNFR1(-/-) mice continue to form proliferating clusters for 6-9 mo. In contrast, DC derived from wild-type, TNFR2(-/-), or TNFR1/2(-/-) mice survived for only 3-4 wk. DC obtained from these TNFR1(-/-) long term cultures (LTC) mice show an unusual mixed immature/mature phenotype. The continuous proliferation of the LTC is GM-CSF dependent and correlates with decreased protein levels of the cyclin-dependent kinase inhibitors p27(KIP1) and p21(CIP1). Prolonged survival of TNFR1(-/-) DC appears to be independent from NF-kappaB and Bcl-2 pathways and is rather enabled by the down-regulation of CD95, resulting in the resistance to CD95 ligand-induced apoptosis. These data point to proapoptotic signals mediated via TNFR1 and antiapoptotic signals mediated via TNFR2 in DC.
[Four perspectives on women's breasts].
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[Where did the opinion disappear?].
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[VLCD a safe and simple treatment of obesity].
This review summarizes Swedish experience with VLCD (Very Low Calorie Diets). VLCD-treatment is a safe and relatively simple way to induce weight reduction in obese patients. The rapid and profound initial weight loss reduces cardiovascular risk factors and relieves obesity-associated symptoms. Weight loss on the order of 20-25 kg is common after 12-16 weeks of treatment. The long-term results, about 10% weight reduction after two years, are similar to what can be expected with pharmacological treatment. VLCD's should be incorporated into long-term treatment programs including diet, physical exercise and lifestyle modification. A team of nurses and/or dieticians can, to a large extent, manage a VLCD-program, restricting the need for involvement of the physician.
[H2 receptor blockaders and weight control].
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[A comment: the core question for obese persons is quality of life. The Malmö study should not result in therapeutic nihilism].
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[Drug therapy of obesity--from bitter experiences to future possibilities].
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[The "father" of cornflakes was a physician--he created a gigantic health resort for the rich America].
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[A referral for exercise? No shortage of life style programs in the databases, but the information can't be efficiently used in practice].
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Culture of bone marrow cells in GM-CSF plus high doses of lipopolysaccharide generates exclusively immature dendritic cells which induce alloantigen-specific CD4 T cell anergy in vitro.
Dendritic cells (DC) can be generated from mouse bone marrow (BM) in the presence of granulocyte-macrophage colony-stimulating factor (GM-CSF). Bacterial stimuli such as endotoxin / lipopolysaccharide (LPS) can induce their final maturation. When BM-DC cultures were treated at day 6 or later with LPS, this final maturation was induced in vitro within 24 h. Such mature DC exhibited high levels of surface MHC II molecules and potent T cell sensitizing, but reduced endocytosis capacity. In contrast, immature DC express only few MHC II molecules and are weak T cell stimulators but highly endocytic. When BM-DC cultures in GM-CSF were treated with 1 microg / ml LPS at day 0 of the culture or throughout the culture, only immature DC developed as defined by phenotype (MHC II low) and function (high endocytosis, weak primary mixed lymphocyte reaction). Those early LPS-treated immature DC induced alloantigen-specific anergy of CD4(+) T cells in vitro. These findings might contribute to the understanding of reduced T cell immunity in the course of septic shock and find application in DC-mediated tolerogenic immunotherapy strategies.
Immature dendritic cells generated with low doses of GM-CSF in the absence of IL-4 are maturation resistant and prolong allograft survival in vivo.
Dendritic cells (DC) were cultured from mouse bone marrow (BM) progenitors in low concentrations of granulocyte-macrophage colony-stimulating factor (GM-CSF) (GM(lo) DC) by two different protocols. The phenotype and functional properties of these GM(lo) DC were compared to those of standard BM-DC cultures generated in high concentrations of GM-CSF (GM(hi) DC) or in low GM-CSF plus IL-4 (GM(lo)/IL-4 DC). An effect of IL-4 on maturation was observed only at low but not high doses of GM-CSF. Compared to mature DC, GM(lo) DC were phenotypically immature, weak stimulators of allogeneic and peptide-specific T cell responses, but substantially more potent in presentation of native protein. Immature GM(lo) DC were resistant to maturation by lipopolysaccharide, TNF-alpha or anti-CD40 monoclonal antibodies, as the expression of co-stimulatory molecules was not increased, and stimulatory activity in oxidative mitogenesis was not enhanced. These maturation-resistant immature GM(lo) DC induced T cell unresponsiveness in vitro and in vivo. GM(lo) DC also prolonged haplotype-specific cardiac allograft survival (from 8 days to >100 days median survival time) when they were administered 7 days (but not 3, 14 or 28 days) before transplantation. Our findings may have important implications for future studies in T cell tolerance induction in vivo.
Excessive fat accumulation is associated with the TNF alpha-308 G/A promoter polymorphism in women but not in men.
AIMS/HYPOTHESIS: Tumour necrosis factor alpha (TNF alpha) is a candidate gene for the development of obesity, which in turn is a major risk factor for diabetes mellitus. The aim of our study was to investigate whether a previously known NcoI-sensitive polymorphism (-308 G/A) in the promoter region of the TNF alpha gene was related to body weight. METHODS: Genotyping was done in 239 male and 342 female non-diabetic subjects with a marked variation in body mass index (BMI). RESULTS: We found three genotypes; AA (n = 13), AG (n = 158) and GG (n = 410). When the material was divided according to sex, allele specific phenotypic differences were confined to women. The female subjects carrying the AA genotype were markedly more obese than both the AG and GG carriers (mean BMI = 41.4 vs 32.3 and 31.7 kg/m2, respectively, p = 0.02). The body fat content of female AA carriers was increased by one-third compared with AG/GG carriers (p = 0.02). We found no differences between genotypes with respect to waist-to-hip ratio, blood pressure or metabolic variables. Among obese female subjects (BMI > 27 kg/m2), we also found that the BMI and body fat content of AA carriers (n = 7) were also higher than for AG/GG carriers. CONCLUSION/INTERPRETATION: The AA-variant at position -308 in the promoter region of the TNF alpha gene could be an important genetic factor behind excessive fat accumulation in women.
Supervised physical activity in Sweden: in theory and practice.
The aim of this study was to assess to which extent community-run projects including physical activity could be identified, described and analysed in terms of objectives, organisation, evaluation and financing, as a resource in prevention and treatment of common lifestyle-related medical problems. The Swedish database Spriline was used as a main source of information. Identification of ongoing Swedish activities was followed by a mail questionnaire. In total, 151 projects were eventually identified. A semistructured questionnaire containing about 30 questions was mailed to the individual listed as responsible for the project, with a reminder 2 months later. Only 52 projects were viable; a follow-up of nonresponders showed that no relevant activity program had ever existed or that the person responsible had left. Walking, aerobics and water activities were the dominating types of activity. Most projects addressed both sexes, but eight weight reduction programs were designed for women only. Evaluation ranged from 'measuring attendance' to 'scientific evaluation'. Physical activity programs may not be as systematically organised as the Swedish database suggests and cannot generally be relied upon as support in patient care, unless critically evaluated in advance.