Obesity and osteoporosis are both common conditions with high rates of morbidity and mortality. There is a relationship between obesity and bone. There are multiple factors that influence the risk of ...fracture, including the quality of bone, the risk of falls, and the padding around the bone. These multiple factors partly explain the finding that obesity protects against fractures in some sites while increasing the risk in other parts of the body. While it is well known that increased weight builds bone, there are several mechanisms related to the obese state that make the bone more fragile. These include the increased production of bone marrow fat cells at the expense of bone-forming osteoblasts, an increase in inflammatory cytokines leading to the activation of bone-resorbing osteoclasts, mutations in the
FTO gene, and obesity-induced increased osteoblast senescence. Surprisingly, the relationship between bone and obesity is not unidirectional; there is now evidence that osteocytes are able to regulate body weight by acting as weighing machines.
Obesity is always genetic or epigenetic in origin in an obesogenic environment. Dietary therapy is required for weight loss. Drugs to suppress hunger and increase satiety may assist while losing ...weight and are essential for most patients in the weight maintenance period. A combination of drugs may be needed. A personalised approach must be used when selecting the appropriate weight loss drug for the patient. This considers possible contraindications, the method of administration and adverse effects, and includes discussing the cost of the treatment. Several drugs do not have an approved indication in Australia for weight loss.
In this study, the levels of circulating mediators of appetite that change after weight loss and promote weight regain did not revert to the values recorded before weight loss. Long-term strategies ...to counteract these changes may be needed to prevent obesity relapse.
Worldwide, there are more than 1.5 billion overweight adults, including 400 million who are obese.
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Although dietary restriction often results in initial weight loss, the majority of obese dieters fail to maintain their reduced weight.
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Understanding the barriers to maintenance of weight loss is crucial for the prevention of relapse.
Body weight is centrally regulated, with peripheral hormonal signals released from the gastrointestinal tract, pancreas, and adipose tissue integrated, primarily in the hypothalamus, to regulate food intake and energy expenditure.
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The number of identified peripheral modulators of appetite is expanding rapidly and includes leptin, ghrelin, cholecystokinin, peptide YY, insulin, pancreatic . . .
Evaluating the glucose tolerance test in mice Andrikopoulos, Sofianos; Blair, Amy R; Deluca, Nadia ...
American journal of physiology: endocrinology and metabolism,
12/2008, Letnik:
295, Številka:
6
Journal Article
Recenzirano
University of Melbourne Department of Medicine (Austin Health/Northern Health), Heidelberg Repatriation Hospital, Heidelberg Heights, Victoria, Australia
Submitted 21 July 2008
; accepted in final ...form 18 September 2008
The objective of this study was to determine the optimal conditions under which to assess glucose tolerance in chow- and high-fat-fed C57BL/6J mice. Mice were fed either chow or high-fat diet for 8 wk. Variables tested were fasting duration (0-, 3-, 6-, and 24-h and overnight fasting), route of administration (intraperitoneal vs. oral) load of glucose given (2, 1, or 0.5 g/kg and fixed 50-mg dose), and state of consciousness. Basal glucose concentrations were increased in high-fat- compared with chow-fed mice following 6 h of fasting (9.1 ± 0.3 vs. 7.9 ± 0.4 mmol/l P = 0.01). Glucose tolerance was most different and therefore significant ( P = 0.001) in high-fat-fed mice after 6 h of fasting (1,973 ± 96 vs. 1,248 ± 83 mmol·l –1 ·120 min –1 ). The difference in glucose tolerance was greater following an OGTT (142%), in contrast to an IPGTT, with a 127% difference between high fat and chow. We also found that administering 2 g/kg of glucose resulted in a greater level of significance ( P = 0.0008) in glucose intolerance in high-fat- compared with chow-fed mice. A fixed dose of 50 mg glucose regardless of body weight was enough to show glucose intolerance in high-fat- vs. chow-fed mice. Finally, high-fat-fed mice showed glucose intolerance compared with their chow-fed counterparts whether they were tested under conscious or anesthetized conditions. We conclude that 2 g/kg glucose administered orally following 6 h of fasting is best to assess glucose tolerance in mice under these conditions.
intraperitoneal glucose tolerance test; oral glucose tolerance test; fasting; high-fat feeding; C57BL/6J
Address for reprint requests and other correspondence: S. Andrikopoulos, Univ. of Melbourne, Dept. of Medicine (AH/NH), Heidelberg Repatriation Hospital, 300 Waterdale Road, Heidelberg Heights, Victoria, Australia (e-mail: sof{at}unimelb.edu.au )
Guidelines recommend gradual weight loss for the treatment of obesity, indicative of a widely held opinion that weight lost rapidly is more quickly regained. We aimed to investigate the effect of the ...rate of weight loss on the rate of regain in obese people.
For this two phase, randomised, non-masked, dietary intervention trial in a Melbourne metropolitan hospital, we enrolled 204 participants (51 men and 153 women) aged 18–70 years with a BMI between 30 and 45 kg/m2. During phase 1, we randomly assigned (1:1) participants with a block design (block sizes of 2, 4, and 6) to account for sex, age, and BMI, to either a 12-week rapid weight loss or a 36-week gradual programme, both aimed at 15% weight loss. We placed participants who lost 12·5% or more weight during phase 1 on a weight maintenance diet for 144 weeks (phase 2). The primary outcome was mean weight loss maintained at week 144 of phase 2. We investigated the primary outcome by both completers only and intention-to-treat analyses. This study is registered with the Australian New Zealand Clinical Trials Registry, number ACTRN12611000190909.
200 participants were randomly assigned to the gradual weight loss (n=103) or rapid weight loss (n=97) programme between Aug 8, 2008, and March 9, 2010. After phase 1, 51 (50%) participants in the gradual weight loss group and 76 (81%) in the rapid weight loss group achieved 12·5% or more weight loss in the allocated time and started phase 2. At the end of phase 2, both gradual weight loss and rapid weight loss participants who completed the study (n=43 in gradual weight loss and n=61 in rapid weight loss) had regained most of their lost weight (gradual weight loss 71·2% regain, 95% CI 58·1–84·3 vs rapid weight loss 70·5%, 57·8–83·2). Intention-to-treat analysis showed similar results (gradual weight loss 76·3% regain, 95% CI 65·2–87·4 vs rapid weight loss 76·3%, 65·8–86·8). In phase 1, one participant in the rapid weight loss group developed cholecystitis, requiring cholecystectomy. In phase 2, two participants in the rapid weight loss group developed cancer.
The rate of weight loss does not affect the proportion of weight regained within 144 weeks. These findings are not consistent with present dietary guidelines which recommend gradual over rapid weight loss, based on the belief that rapid weight loss is more quickly regained.
The Australian National Health and Medical Research Council and the Sir Edward Dunlop Medical Research Foundation.
Although weight loss can usually be achieved by restricting food intake, the majority of dieters regain weight over the long-term. In the hypothalamus, hormonal signals from the gastrointestinal ...tract, adipose tissue and other peripheral sites are integrated to influence appetite and energy expenditure. Diet-induced weight loss is accompanied by several physiological changes which encourage weight regain, including alterations in energy expenditure, substrate metabolism and hormone pathways involved in appetite regulation, many of which persist beyond the initial weight loss period. Safe effective long-term strategies to overcome these physiological changes are needed to help facilitate maintenance of weight loss. The present review, which focuses on data from human studies, begins with an outline of body weight regulation to provide the context for the subsequent discussion of short- and long-term physiological changes which accompany diet-induced weight loss.
BACKGROUND: Weight regain after weight loss may not be due primarily to voluntary return to social habits but may be explained by changes in peripheral hormonal signals activating hunger and ...encouraging feeding behavior. OBJECTIVE: The objective of this study was to investigate physiologic adaptations to weight loss that may encourage weight regain. DESIGN: The study had a within-subject repeated-measure design 12 healthy, obese men, 33-64 y, body mass index (in kg/m²) 30-46 and was a clinical intervention investigation of circulating metabolites and hunger-satiety responses before and after weight loss. Measures included anthropometry (bioelectrical impedance, body weight, and waist circumference), concentrations of circulating hormones and metabolites ketone bodies, free fatty acids (FFAs), insulin, leptin, glucose, and cholecystokinin (CCK), and measures of hunger and satiety at baseline, 8 wk after weight loss with a very-low-energy diet, and 1 wk after weight maintenance. RESULTS: Weight loss led to a reduction in postprandial CCK secretion (P = 0.016). However, when subjects were ketotic (elevated circulating β-hydroxybutyrate concentrations), CCK secretion was sustained at concentrations before weight loss. After weight loss, there were reduced postprandial FFA concentrations (P = 0.0005). The presence of ketosis sustained FFA to concentrations before weight loss (P = 0.60). CONCLUSION: Rapid weight loss of almost equal to10% of initial body weight results in a reduction in postprandial CCK and FFA concentrations.
Controlling obesity has become one of the highest priorities for public health practitioners in developed countries. In the absence of safe, effective and widely accessible high-risk approaches (e.g. ...drugs and surgery) attention has focussed on community-based approaches and social marketing campaigns as the most appropriate form of intervention. However there is limited evidence in support of substantial effectiveness of such interventions.
To date there is little evidence that community-based interventions and social marketing campaigns specifically targeting obesity provide substantial or lasting benefit. Concerns have been raised about potential negative effects created by a focus of these interventions on body shape and size, and of the associated media targeting of obesity.
A more appropriate strategy would be to enact high-level policy and legislative changes to alter the obesogenic environments in which we live by providing incentives for healthy eating and increased levels of physical activity. Research is also needed to improve treatments available for individuals already obese.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
Obesity is the major modifiable risk factor for osteoarthritis (OA). A major focus of management in OA is weight loss. Although we live in an obesogenic environment, obesity has a predominantly ...genetic and epigenetic basis. This explains a person's weight set point which is defended by biological mechanisms making weight loss difficult to achieve and maintain long term, regardless of the methods used. Significant weight regain occurs after weight loss, with weight tending to return to pre-treatment levels after cessation of interventions including the glucagon-like peptide-1 (GLP-1) agonists. An area that has received little attention is the slow, insidious weight creep of 0.5–1 kg/year over adulthood that sees individuals relentlessly increase weight. There is evidence that low intensity, personalised lifestyle interventions can prevent this weight creep, providing patients with achievable goals. In this narrative review, we examine the evidence for weight loss in OA, the biological mechanisms that make weight loss difficult to achieve and maintain and the potential negative impacts on patients. We review the evidence for preventing weight gain, the improvement in patient outcomes and the potential for significant healthcare savings through reduced knee replacements. We propose a combined approach of weight loss when indicated, together with targeting weight creep across adult years and the potential role of metformin. Implementing these combined approaches is likely to be more effective in improving patient related outcomes, reducing joint damage and healthcare costs, than our current focus on achieving weight loss in OA.
A cross-sectional study.
To determine whether body composition is associated with low back pain intensity and/or disability.
The relationship between obesity and low back pain and disability is ...unclear. No study has examined the role of body composition in low back pain and disability.
A total of 135 participants (25-62 years), with a range of body mass indices (18-55 kg/m), were recruited for a study examining the relationship between obesity and musculoskeletal disease. Participants completed the Chronic Back Pain Grade Questionnaire, which examines individuals' levels of low back pain intensity and disability. Body composition was assessed using dual radiograph absorptiometry.
Body mass index was associated with higher levels of back pain intensity (Odds ratio OR = 1.35; 95% confidence interval CI = 1.09, 1.67) and disability (OR = 1.66; 95% CI = 1.31, 2.09). Higher levels of pain intensity were positively associated with total body (OR = 1.19; 95% CI = 1.04, 1.38) and lower limb fat mass (OR = 1.51; 95% CI = 1.04, 2.20), independent of lean tissue mass. There were also positive associations between higher levels of low back disability and total body (OR = 1.41; 95% CI = 1.20, 1.67) and upper (OR = 1.67; 95% CI = 1.27, 2.19) and lower (OR = 2.29; 95% CI = 1.51, 3.49) limbs fat mass. Similar relationships were observed with trunk, android, and gynoid fat mass. After adjusting for confounders, no measures of lean tissue mass were associated with higher pain intensity or disability (P > 0.10).
Greater fat, but not lean tissue mass, was associated with high levels of low back pain intensity and disability. Longitudinal investigation is needed to determine whether fat mass is predictive of low back pain and disability, as this may have important implications for further prevention strategies. Understanding the mechanism for these relationships may provide novel approaches to managing low back pain.
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