The objective of this study was to explore the perception of, feelings and attitudes toward overweight or obesity, and the perceived barriers to weight loss among native adults from lower socio-economic background. A total of six gender- and ethnic-specific focus groups consisted of 38 overweight and obese purposefully and criterion selected adults (21 women and 17 men), participated in this study. An unstructured discussion guide based on the study objectives were used for the focus groups. The results showed that some participants perceived themselves as ugly, felt ashamed of their body size and were frustrated because they did not desire to be overweight. Due to their excess weight, most also expressed they were less effective in their work performances. Although some participants had negative attitudes toward themselves because of excess weight, this appeared to link to self-stigmatization rather than anti-obesity discrimination. The participants remained in the Pre-contemplation stage of losing weight probably because of perceived barriers such as difficulty to resist eating, lack of know how and previous failed attempts to lose weight. Importantly, this study provided some evidence that individuals in the Pre-contemplation stage are unable to take action to lose weight, even if effective strategies are suggested.
We report a case of systemic lupus erythematosus complicated by transverse myelopathy and hyperphagia. To our knowledge the latter has not been reported before.
REM sleep is a crucial component of sleep. Animal studies indicate that rapid eye movement (REM) sleep deprivation elicits changes in gene expression. Down regulatory antagonist modulator (DREAM) is a protein which downregulates other gene transcriptions by binding to the downstream response element site. The aim of this study is to examine the effect of REM sleep deprivation on DREAM expression in ventrobasal thalamic nuclei (VB) of rats. Seventy-two male Sprague-Dawley rats were divided into four major groups consisting of free-moving control rats (FMC) (n = 18), 72-h REM sleep-deprived rats (REMsd) (n = 18), 72-h REM sleep-deprived rats with 72-h sleep recovery (RG) (n = 18), and tank control rats (TC) (n = 18). REM sleep deprivation was elicited using the inverted flower pot technique. DREAM expression was examined in VB by immunohistochemical, Western blot, and quantitative real-time polymerase chain reaction (qRT-PCR) studies. The DREAM-positive neuronal cells (DPN) were decreased bilaterally in the VB of rats deprived of REM sleep as well as after sleep recovery. The nuclear DREAM extractions were increased bilaterally in animals deprived of REM sleep. The DREAM messenger RNA (mRNA) levels were decreased after sleep recovery. The results demonstrated a link between DREAM expression and REM sleep deprivation as well as sleep recovery which may indicate potential involvement of DREAM in REM sleep-induced changes in gene expression, specifically in nociceptive processing.
We examined the effects of liraglutide, a glucagon-like peptide-1 analogue on appetite and plasma ghrelin in non-diabetic obese participants with subclinical binge eating (BE). Forty-four obese BE participants (mean age: 34±9 years, BMI: 35.9±4.2kg/m(2)) were randomly assigned to intervention or control groups for 12 weeks. All participants received standard advice for diet and exercise. Binge eating score, ghrelin levels and other anthropometric variables were evaluated at baseline and at the end of the study. Participants who received liraglutide showed significant improvement in binge eating, accompanied by reduction in body weight, BMI, waist circumference, systolic blood pressure, fasting glucose and total cholesterol. Ghrelin levels were significantly increased which may potentially diminish the weight loss effects of liraglutide beyond the intervention.
Introduction: Childhood obesity is increasing in prevalence in Malaysia. Excess in dietary intake and inadequate physical activity contribute to the development of obesity among children. The objective of this study was to de-termine the association between eating behaviour and excess weight among primary school children in an urban community in Malaysia. Methods: This is a baseline data of a randomized control field trial of a family-based inter-vention to reduce adiposity in overweight and obese children. It involved five primary government schools in Bandar Baru Bangi, Selangor. The inclusion criteria include parent-child dyad; children aged 7 to 10 years with body mass index (BMI) z-score of +1 standard deviation or more. Parents completed the validated self-administered Children Eating Behaviour Questionnaire (CEBQ). This questionnaire assessed children’s eating behaviour that includes food responsiveness, enjoyment of food, emotional overeating, desire to drink, slowness in eating, satiety responsiveness, emotional undereating and food fussiness. The children’s weight and height were measured and the BMI z-score was calculated. The association between CEBQ subscales and obesity was assessed using multiple linear regression, adjusted for sex and family income. Results: One hundred and thirty-four parent-child dyads had participated in this study. The food responsiveness was found to be significant with excess weight (β = 0.094, 95% CI: 0.02-0.17, p= 0.014). Conclusion: The food responsiveness subscale was associated with excess weight. This eating behaviour need to be taken into consideration in the development and implementation of health campaign targeted at the re-duction of childhood obesity.
Klüver-Bucy syndrome was first diagnosed in humans in 1955, after a group
of people who had experienced temporal lobectomy. It is a rare
neuropsychiatry disease and of which little is understood about its
pathophysiological processes. Here we present a 60-year-old man seen in the
outpatient psychiatric department in a tertiary hospital in Kuala Lumpur
who presented to us with hyper sexuality, impulsivity, docility, amnesia and
hyperphagia for the past 10 months. He was diagnosed with Herpes Simplex
Virus with encephalitis 18 months ago and was shown to have bilateral
meningoencephalitis of his temporal lobes. Thus, a diagnosis of Klüver-Bucy
was made. We have taken a multi-disciplinary team approach to treat his
illness and specific goals has been laid out in each discipline. A written
consent has been taken by the patient and his family for the publication of
this report.
Introduction: Polymetabolic syndrome is a malady encompassing centralized accumulation of lipids and subsequent resistance to insulin leading towards diabesity. Currently, this condition is perilous threat to public health and also, creating perplexity for medical scientists. There is an intensive need for the development of obese rodent model having close resemblance with human metabolic syndrome (MetS); so that intricate molecular and/or therapeutic
targets can be elucidated. The resultant simulations will be beneficial to explicate not only pathogenesis but also secret conversation of signaling pathways in inducing MetS related complications in other organs. Methods: Currently, there are different methods for the development of rodent models of MetS, for instance, utilizing high lipogenic diet, genetic alterations, induction by chemicals or by combination of high fat diet and few others. In general, combination of cafeteria or western diet and low dose of streptozotocin (STZ) is a fine example of diet induced experimental model. In this model animals are allowed free access to highly palatable, energy dense, unhealthy human food for 12-18 weeks which promotes voluntary hyperphagia resulting in weight gain, increased fat mass and insulin resistance. At the end of feeding period 30mg/kg STZ is given intraperitoneally to mimic human type 2 diabetic condition.
Conclusion: Consumption of cafeteria diet with low dose STZ is considered to be the robust model of diabesity offering an exceptional stage to investigate the genomic, molecular, biochemical and cellular mechanisms of obesity and type 2 diabetes.
Leptin, a 167 amino-acid product of the ob or LEP gene, was first reported in 1994 after a 40-year search that began following the emergence of a mutant strain of mice with hyperphagia, early on-set obesity, and delayed sexual maturation. Since then, leptin deficiency has also been reported in the rat, and more recently in humans. It is secreted constitutively primarily by the white adipose tissue, and in smaller quantities by a number of non-adipose tissues. It acts by binding to specific membrane bound leptin receptors, belonging to the class 1 cytokine receptor family, and activating the JAK-STAT system. Leptin regulates appetite and body weight mainly through its actions on the hypothalamus involving the NPYmelanocortin pathway, and, to a lesser extent, through increased energy expenditure by way of sympathoactivation and increased substrate cycling. Its effects on reproduction, puberty in particular, are mediated through actions on the hypothalamic-pituitary-gonadal axis and on the gonads. Leptin also appears to have permissive roles in CNS development during the neonatal period, bone growth and development, and in haemopoietic and immune functions. Although it was its deficiency state that first led to its discovery, it now appears that the clinical significance of leptin lies not only in the consequences of its deficiency but also when it is in excess as occurs in obesity. Emerging evidence is implicating leptin as a link between obesity associated cardiovascular disease risks and infertility. Besides this, leptin is also being implicated as a growth factor in cancer. The story that started with a search for a body weight regulating factor is now unfolding into one that is revealing roles for leptin that stretch beyond the regulation of appetite and body weight.
Food is closely related with emotion. It often provides comfort and satisfaction. Some individuals choose to turn to food to curb their negative emotion, resulting in disturbances in
eating patterns, such as overeating which lead to obesity and severely controlling food intake, which culminate in eating disorders like anorexia nervosa, bulimia nervosa and binge eating. These disorders are not related to the eating problems per se but often due to underlying or complicated by psychological factors, namely depression, anxiety, impulse control problems and personality. The roles of psychological factors in eating disorders and obesity should therefore not be downplayed. These disorders should be managed comprehensively involving multiple approaches, including not only biological but also psychological interventions provided by a professional team comprising endocrinologists, psychiatrists, dietitians, exercise physicians and surgeons.
Hyperadrenocorticism is the excessive production of cortisol by the adrenal cortex. 15-20% of hyperadrenocorticism in dogs may be due to functional adrenal tumour. Here we present a case of functional adrenal tumour in a 10 years old Shih-Tzu Poodle mixed-breed dog that was presented to University Veterinary Hospital, Universiti Putra Malaysia. Physical examination findings include multiple cutaneous myiasis, a pendulous abdomen with comedones on the ventral thoracic region and thinning of the skin. Clinical signs shown were polyuria, polydipsia and polyphagia. Serum biochemistry result showed elevated alkaline phosphatase enzyme of 5 folds. Urinary specific gravity was minimally concentrated (1.015). Radiography showed generalised hepatomegaly. Meanwhile, ultrasonography showed unilateral enlargement of the right adrenal gland with mineralisation. Invasion of the right adrenal gland into the caudal vena cava was observed. A differentiation test (high-dose dexamethasone suppression test) was performed and a lack of suppression of the cortisol level was observed. Based on the appropriate clinical signs and physical examination findings, elevated alkaline phosphatase enzyme, minimally concentrated urinary specific gravity, generalised hepatomegaly, unilateral adrenal gland enlargement, and high-dose dexamethasone suppression test, a diagnosis of functional adrenal tumour was made.