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Biomedical subjects

Ingrid Schmidt

Publications and source records attributed to Ingrid Schmidt.

13 recordsLinked to original sources
PubMed2006

Effects of periodic intake of a high-caloric diet on body mass and leptin resistance.

The effects of continuous or intermittent access to a high-caloric (HC) diet, always offered in addition to standard chow, on body mass and leptin resistance were analyzed in female C57BL/6J mice. Susceptibility for diet-induced obesity (DIO) was apparent from the marked preference for the HC diet. Continuous HC diet feeding of mice at 4 weeks of age induced leptin resistance within 2 weeks and massive gains in body mass, although with increasing inter-individual variability in the inbred strain considered to be isogenic. In adult mice receiving HC diet for the first time, leptin treatment failed to reduce energy intake first after 11 days of HC diet feeding, but became effective again within 3 days after HC diet withdrawal. In mice with a history of several preceding periods of access to the HC diet totalling >30 days, supplementary HC diet abolished the anorectic effect of leptin treatment within only 3 days and it reappeared not earlier than 11 days after HC diet withdrawal. Thus, in the investigated DIO-prone mouse strain both, the loss of responsiveness to leptin under HC diet and its recovery after HC diet withdrawal strongly depended on the dietary history. Recovery from leptin resistance during periods of intermittent chow feeding was associated with losses of body mass that did not completely compensate for the obesity-inducing effect of the preceding HC diet.

Age Factors↗
PubMed2005

Dose-related steady states of fat loss in long-term leptin-treated ob/ob mice: leptin resistance or desensitization versus counterregulatory signaling.

We tried to unravel why leptin's fat store depleting action levels off in the course of long-term applications. Supplying leptin by minipump infusion for 2 months to ob/ob mice at rates between 115 pmol day(-1) and 460 pmol day(-1) resulted in stable plasma leptin levels between 0.2 ng ml(-1) and 8 ng ml(-1). Initial treatment effects were leptin dose-dependent reductions in food intake and body mass, especially in fat content, followed by re-increases of food intake to levels only 4-18% below pre-treatment levels. Decreased body mass subsequently stabilized dose-dependently with body fat contents between 4% and 33% showing that total fat depletion was not a precondition for the progressive reduction of leptin-induced anorexia. Oxygen consumption measurements excluded contributions of enhanced energy dissipation to fat depletion. Plasma insulin concentrations declined from excessively high pre-treatment levels to steady, leptin dose-dependent levels within the normal range. Temporary anorexia in response to repeated additional 1-day leptin injections (100 pmol g(-1) day(-1)) remained unchanged throughout long-term leptin infusion. Among various alternatives considered to explain the adipostatic equilibrium attained at new, dose-dependent levels under long-term leptin treatment, interaction between the leptin signal and at least one counteracting signal increasing with fat depletion is proposed as the most plausible working hypothesis.

Adipose Tissue↗
PubMed2005

Gender equity in health care in Sweden--minor improvements since the 1990s.

A report by the Swedish National Committee on Gender Disparities in Patient Care (1996) identified many shortcomings in the ability of the health sector to gear patient management and treatment to the specific needs of men and women. To promote gender equity in health care, the Committee presented several proposals relating to research, education, monitoring, and evaluation of health services and the responsibilities of health authorities. In 2002, the Swedish Government authorised the National Board of Health and Welfare to review and analyse gender equity trends in health care. Data from, e.g. the national quality registers, epidemiological health data registers, population surveys, and Patient Trust Boards were compiled to identify gender disparities in the quality and accessibility of health services. The curricula of medical universities and the policies of major research funds were reviewed, as were developments in major fields of health research. The National Board found that many of the gender disparities identified in the 1990s still exist, e.g. access to advanced evidence-based technologies such as coronary interventions. As previously, women account for around 60%, and men for 40%, of complaints, e.g. to the Patients' Advisory Committees. Many of the proposals of the National Committee have not been fully implemented by the national authorities or the county councils. We conclude that promoting gender equity in health care is an important but difficult task for health authorities. To make health services more gender sensitive a combination of strategies, including enforcement by guidelines and regulations, may be needed.

Female↗
PubMed2003

Age-dependent hypothalamic expression of neuropeptides in wild-type and melanocortin-4 receptor-deficient mice.

In young (35- to 56-day-old) and middle-aged (9-mo-old) wild-type (+/+) and melanocortin-4 receptor (MC4R)-deficient (+/-, -/-) mice, expressions of neuropeptide Y (NPY), agouti-related protein (AGRP), pro-opiomelanocortin (POMC), and cocaine-and-amphetamine-regulated transcript (CART) were analyzed in the arcuate nucleus (ARC) and adjacent regions comprising the dorsomedial (DMN) and ventromedial (VMN) nucleus. In the ARC of young mice, NPY and AGRP expression increased and POMC and CART expression decreased with body fat content. Adjusting for the influence of body fat content by ANCOVA showed that the levels of NPY, POMC, and CART were highest and of AGRP lowest in young -/- mice. In the middle-aged mice, feedback from body fat content was weakened. For -/- mice ANCOVA revealed higher NPY and AGRP, lower POMC, and unchanged CART expression levels relative to young -/- mice. In the DMN and VMN, POMC and AGRP signals were absent at each age. CART was expressed in the DMN independent of age, fat content, and genotype. For NPY expression, an age-dependent induction was found in the DMN and VMN; it was absent in the young but present in the middle-aged mice, showing close positive correlations between body fat content and the numbers of NPY-labeled cells which were further enhanced in -/- mice. Thus MC4R deficiency augments age-induced NPY expression in the DMN and VMN with no feedback from body fat content. Negative feedback control by body fat content on ARC neuropeptide expression is present in young animals but vanishes with age and is modulated by MC4R deficiency.

Adipose Tissue↗
PubMed2003

Hyperphagia, not hypometabolism, causes early onset obesity in melanocortin-4 receptor knockout mice.

Previous studies on mice with melanocortin-4 receptor gene (MC4r) knockout have focused on obese adults. Because humans with functional MC4r mutations show early-onset obesity, we determined the onset of excessive fat deposition in 10- to 56-day-old mice, taking into account sex and litter influences. Total body fat content of MC4r-/- on day 35 and MC4r+/- on day 56 significantly exceeds that of MC4r+/+. Plasma leptin levels increase in proportion to fat mass. According to cumulative food intake and energy expenditure measurements from day 21 to 35, onset of excessive fat deposition in MC4r-/- is fueled by hyperphagia and counteracted partially by hypermetabolism. In 35- to 56-day-old mice, arcuate nucleus neuropeptide Y (NPY) mRNA decreases and pro-opiomelanocortin (POMC) mRNA increases with fat content and plasma leptin levels independently of genotype. Taking into account fat content by ANCOVA reveals, however, increases in both NPY mRNA and POMC mRNA due to melanocortin-4 receptor (MC4R) deficiency. We conclude that hyperphagia, not hypometabolism, is the primary disturbance initiating excessive fat deposition in MC4R-deficient mice at weaning and that the overall changes in NPY and POMC expression tend to antagonize the onset of excessive fat deposition.

Adipose Tissue↗
PubMed2003

Family members' perceptions of pain and distress related to analgesics and psychotropic drugs, and quality of care of elderly nursing home residents.

The aims of the present study were: (1) to describe family members' perceptions of nursing homes residents' pain and distress in relation to analgesics and psychotropic drugs; and (2) to compare whether background variables, dementia, help/support, prescribing of analgesics and psychotropic drugs, and quality of care vary between subgroups of residents. Two hundred and thirty-two family members of elderly people in 10 Swedish nursing homes participated in the study. The participants responded to a questionnaire including background variables, pain and distress variables, and the Quality from the Patient's Perspective (QPP) questionnaire. Data on drug prescribing was obtained from the medical records. The head nurse on each ward noted whether or not the resident had a documented or known diagnosis of dementia. The results showed that a high frequency of elderly nursing home residents were estimated as having physical pain and worry. A large number of the residents were prescribed psychotropic drugs. In addition, some of the residents with moderate or severe physical pain were not prescribed any analgesics. The residents were divided into three subgroups based on scores of physical discomfort, physical pain and worry. Subgroup comparisons differed with regard to sex, help/support, drugs and quality of care. Staff have a responsibility to assess the residents' pain and distress since this will form a basis for better pain and distress management. Other suggestions for improving quality of care are the provision of better information to the family members and the residents, meaningful occupation, less task-oriented care, and care that involves residents.

Aged↗
PubMed2002

Developmental and food-access-dependent changes in effector systems activated by leptin.

In small mammals leptin reduces fat stores not only by inhibiting food intake but also by disinhibiting metabolic cold defense. Presuming that postnatal age and feeding regime set the conditions for either mode of leptin action, we compared the caloric equivalents of changes in fat mass, metabolic rate (MR) and food intake (FI) induced by 10-day treatments with leptin, in rats treated from postnatal days 7, 15, 25 onward and in adult mice that were free-feeding or food restricted. Whereas MR changes are known to dominate from postnatal days 7-16, changes in MR explained only about 50% and 30% of the leptin-induced changes in fat mass between days 15-24 and days 25-34, respectively. In adult mice of similar body weights, leptin-induced reductions in fat mass under free-feeding conditions were due only to FI decreases but due only to MR increases under food-restricted conditions. Thus, the same leptin treatment induces the same percentage decrease in body fat content by driving the two effectors differently, depending on age and feeding conditions. Consequently, in assessing the effects of leptin under various physiological conditions, short-term measurements of FI or MR alone are not sufficient. Instead, determination of the resultant decreases in total body fat is required.

Adipose Tissue↗
PubMed2002

Salmon calcitonin - a potent inhibitor of food intake in states of impaired leptin signalling in laboratory rodents.

To compare the anorectic effectiveness of leptin and the amylin analogue salmon calcitonin (sCT), rodents were treated on 1 day with subcutaneous injections. In chow-fed C57Bl/6J mice, leptin and sCT reduced energy intake and acted additively. After C57Bl/6J mice had become leptin-resistant on being fed chocolate as a palatable high-caloric supplement to chow, their sCT-induced decrease in energy intake was more pronounced than in chow-fed mice with differential changes in the intake of chocolate (strong reduction) and chow (slight increase). Dose-response relationships for sCT-induced reductions in energy intake were analysed in chow-fed C57Bl/6J mice and two obese strains, ob/ob mice and melanocortin-4 receptor knockout (MC4-r-KO) mice, as well as in wild-type and fatty (fa/fa) rats. Compared to C57Bl/6J mice, reduction in food intake induced by sCT was attenuated in MC4-r-KO mice, and nearly absent in ob/ob mice, over the dose range investigated. Compared to C57Bl/6J mice, wild-type rats responded more sensitively to sCT and its efficiency was only slightly reduced in fatty (fa/fa) rats. Thus, while genetically induced failures of leptin signalling reduce the action of sCT, it effectively inhibits the intake of a palatable, high fat-high sugar diet even in states of diet-induced obesity with functional leptin resistance.

Animals↗
PubMed2002

MSG lesions decrease body mass of suckling-age rats by attenuating circadian decreases of energy expenditure.

Suckling-age rats display endogenous circadian rhythmicity of metabolic rate (MR) with energy-saving, torpor-like decreases, which are sympathetically controlled and suppressed by leptin treatment. We investigated whether neonatal monosodium glutamate (MSG) treatment, known to cause arcuate nucleus damage and adult-age obesity, alters energy balance in the first two postnatal weeks. Continuously recorded MR and core temperatures (T(c)) show that MSG treatment disinhibits the periodic, sympathetically controlled, energy-saving drops of T(c) and MR. Increased energy expenditure thus explains reduced body fat at normal lean body mass found in MSG-treated pups artificially nourished identically to controls. In MSG-treated mother-reared pups, lean body mass is additionally reduced, suggesting that MSG also reduces suckling. Plasma leptin levels are similar in controls and MSG-treated pups but higher per unit of fat mass in the latter. We conclude that the postweaning development of MSG obesity and depressed thermogenesis are preceded by an early phase of increased energy expenditure with decreased fat deposition during suckling age and hypothesize cell damage in the arcuate nucleus to be involved in both.

Animal Husbandry↗
PubMed2002

Metabolic diseases: the environment determines the odds, even for genes.

The odds for well-being or illness are determined by the interplay of genetic and environmental impacts. In this review, normal and disturbed body weight regulation are used to demonstrate the role of integrative bioresearch in bridging the gap between identified genotypes and an understanding of the functions of redundant and plastic control systems underlying phenotypes.

Animals↗
PubMed2002

Inactivation of the GR in the nervous system affects energy accumulation.

The homeostatic regulation of body weight protects the organism from the negative consequences of starvation and obesity. Glucocorticoids (GCs) modulate this regulation, although the underlying mechanisms remain unclear. To address the role of central GRs in the regulation of energy balance, we studied mice in which GRs have selectively been inactivated in the nervous system. Mutant mice display marked growth retardation. During suckling age this is associated with normal fat deposition causing a 60% temporary increase of percent body fat, compared with control littermates. After weaning, fat and protein depositions are reduced so that adults are both smaller and leaner than their controls. Decreased food intake and, after weaning, reduced metabolic efficiency account for these developmental disturbances. Plasma levels of leptin and insulin, two important energy balance regulators, are elevated in young mutants but normal in adults. Leptin/body fat ratio is higher at all ages, suggesting disturbed control of circulating leptin as a consequence of chronically elevated GC levels in mutant animals. Adult mutants display increased hypothalamic CRH and NPY levels, but peptide levels of melanin concentrating hormone and Orexin A and B are unchanged. The increased levels of plasma GCs and hypothalamic CRH may act as catabolic signals most likely leading to persistently reduced energy accumulation.

Aging↗