Management of obesity in low-income African Americans.
The Bariatrics Clinic at Howard University Hospital was initiated to help low-income African-American adults with low literacy skills in obesity control. Fourteen African-American women and two men participated in the study. Essential components of the treatment included nutrition education, exercise, and behavior modification related to food intake. The nutrition education component involved teaching nutritional needs, taking into account low literacy skills, low economic status, and individual food preferences. A realistic diet plan was based on individual needs, economic status, availability of food, likes and dislikes, lifestyle, and family dynamics. On average, patients lost 2 lb a week on this program. On average, a 14-lb weight loss occurred in seven weeks. There has been a 10% dropout from this program as opposed to drop out rates of 40% to 50% with other treatments. The main reasons for the success of this program is that it is individualized and is sensitive to food preferences. (+info
Gastric surgery for pseudotumor cerebri associated with severe obesity.
OBJECTIVE: To study the efficacy of gastric surgery-induced weight loss for the treatment of pseudotumor cerebri (PTC). SUMMARY BACKGROUND DATA: Pseudotumor cerebri (also called idiopathic intracranial hypertension), a known complication of severe obesity, is associated with severe headaches, pulsatile tinnitus, elevated cerebrospinal fluid (CSF) pressures, and normal brain imaging. The authors have found in previous clinical and animal studies that PTC in obese persons is probably secondary to a chronic increase in intraabdominal pressure leading to increased intrathoracic pressure. CSF-peritoneal shunts have a high failure rate, probably because they involve shunting from a high-pressure system to another high-pressure zone. In an earlier study of gastric bypass surgery in eight patients, CSF pressure decreased from 353+/-35 to 168+/-12 mm H2O at 34+/-8 months after surgery, with resolution of headaches in all. METHODS: Twenty-four severely obese women underwent bariatric surgery--23 gastric bypasses and one laparoscopic adjustable gastric banding--62+/-52 months ago for the control of severe obesity associated with PTC. CSF pressures were 324+/-83 mm H2O. Additional PTC central nervous system and cranial nerve problems included peripheral visual field loss, trigeminal neuralgia, recurrent Bell's palsy, and pulsatile tinnitus. Spontaneous CSF rhinorrhea occurred in one patient, and hemiplegia with homonymous hemianopsia developed as a complication of ventriculoperitoneal shunt placement in another. There were two occluded lumboperitoneal shunts and another functional but ineffective lumboperitoneal shunt. Additional obesity comorbidity in these patients included degenerative joint disease, gastroesophageal reflux disease, hypertension, urinary stress incontinence, sleep apnea, obesity hypoventilation, and type II diabetes mellitus. RESULTS: At 1 year after bariatric surgery, 19 patients lost an average of 45+/-12 kg, which was 71+/-18% of their excess weight. Their body mass index and percentage of ideal body weight had fallen to 30+/-5 kg/m2 and 133+/-22%, respectively. In four patients, less than 1 year had elapsed since surgery. Five patients were lost to follow-up. Surgically induced weight loss was associated with resolution of headache and pulsatile tinnitus in all but one patient within 4 months of the procedure. The cranial nerve dysfunctions resolved in all patients. The patient with CSF rhinorrhea had resolution within 4 weeks of gastric bypass. Of the 19 patients not lost to follow-up, 2 regained weight, with recurrence of headache and pulsatile tinnitus. Additional resolved associated comorbidities were 6/14 degenerative joint disease, 9/10 gastroesophageal reflux disorder, 2/6 hypertension, and all with sleep apnea, hypoventilation, type II diabetes mellitus, and urinary incontinence. CONCLUSIONS: Bariatric surgery is the long-term procedure of choice for severely obese patients with PTC and is shown to have a much higher rate of success than CSF-peritoneal shunting reported in the literature, as well as providing resolution of additional obesity comorbidity. Increased intraabdominal pressure associated with central obesity is the probable etiology of PTC, a condition that should no longer be considered idiopathic. (+info
Regional specificity of ASP binding in human adipose tissue.
Obesity, in particular omental (OM) adiposity, is associated with diabetes and cardiovascular disease. Thus site-specific regulation of fat storage is important to understand. Acylation-stimulating protein (ASP) is a potent stimulator of glucose transport and triglyceride synthesis in adipocytes. In the present study, we characterized receptor binding of 125I-labeled ASP to human adipocyte plasma membranes from paired OM and subcutaneous (SC) sites in normal (N) and obese (O) male (M) and female (F) subjects (n = 24). Overall, specific binding of 125I-ASP was in the order of SC > OM and O > N (in SC tissue, particularly in F). Receptor affinity of 125I-ASP was higher [lower dissociation constant (Kd)] in SC than in OM (63.6 +/- 16.2 vs. 160.7 +/- 38.6 nM, P < 0.02), especially in F (37.0 +/- 11.1 F-N and 26.3 +/- 6.7 nM F-O) and lower (higher Kd) in male OM (291.8 +/- 116.8 M-N and 149.4 +/- 56.4 M-O). The greater binding and higher affinity of 125I-ASP binding to SC suggests that ASP may be an important factor in maintaining regional adipose tissue mass. Conversely, lower binding and receptor affinity in male OM adipose tissue may contribute to the fatty acid imbalance and metabolic complications associated with this syndrome, by reducing the efficiency of adipose fatty acid trapping by the ASP pathway. (+info
A sib-pair analysis study of 15 candidate genes in French families with morbid obesity: indication for linkage with islet 1 locus on chromosome 5q.
As part of an ongoing search for susceptibility genes in obese families, we performed linkage analyses in 101 French families between qualitative and quantitative traits related to morbid obesity and polymorphisms located in or near 15 candidate genes whose products are involved in body weight regulation. These included cholecystokinin A and B receptors (CCK-AR and CCK-BR), glucagon-like peptide 1 receptor (GLP-1R), the LIM/homeodomain islet-1 gene (Isl-1), the caudal-type homeodomain 3 (CDX-3), the uncoupling protein 1 (UCP-1), the beta3-adrenoceptor (beta3-AR), the fatty acid-binding protein 2 (FABP-2), the hormone-sensitive lipase (HSL), the lipoprotein lipase (LPL), the apoprotein-C2 (apo-C2), the insulin receptor substrate-1 (IRS-1), the peroxisome proliferator-activated receptor-gamma (PPAR-gamma), tumor necrosis factor-alpha (TNF-alpha), and the liver carnitine palmitoyltransferase-1 (CPT-1). Phenotypes related to obesity such as BMI, adult life body weight gain, fasting leptin, insulin, fasting glycerol, and free fatty acids were used for nonparametric sib-pair analyses. A weak indication for linkage was obtained between the Isl-1 locus and obesity status defined by a z score over one SD of BMI (n = 226 sib pairs, pi = 0.54 +/- 0.02, P = 0.03). Moreover, a suggestive indication for linkage was found between the Isl-1 locus and BMI and leptin values (P = 0.001 and 0.0003, respectively) and leptin adjusted for BMI (P = 0.0001). Multipoint analyses for leptin trait with Isl-1 and two flanking markers (D5S418 and D5S407) showed that the logarithm of odds (LOD) score is 1.73, coinciding with the Isl-1 locus. Although marginally positive indications for linkage in subgroups of families were found with IRS-1, CPT-1, and HSL loci, our data suggested that these genes are not major contributors to obesity. Whether an obesity susceptibility gene (Isl-1 itself or another nearby gene) lies on chromosome 5q should be determined by further analyses. (+info
Treatment for morbid obesity.
There is no single unifying theory to explain the aetiology of obesity but several environmental factors, such as decreased physical activity and increased fat intake may contribute to its development in genetically predisposed individuals. Dietary and pharmacological treatments of morbid obesity have been proven to be unsuccessful. Modern surgical treatments have been shown to be effective in achieving significant weight loss with consequent reduction in morbidity. Despite the fact that surgical treatment of morbid obesity is the only therapeutic form that has stood the test of time, it still remains a crisis-driven form of therapy in the UK. It is probable that a better understanding of the aetiology and physiology of obesity may lead to the development of an effective pharmacological treatment of obesity in the future. However, until then, surgical treatment of morbid obesity should be considered as an effective and efficient way of treatment in selected cases. (+info
Alteration of the leptin network in late morbid obesity induced in mice by brain infection with canine distemper virus.
Viruses can induce progressive neurologic disorders associated with diverse pathological manifestations, and therefore, viral infection of the brain can impair differentiated neural functions, depending on the initial viral tropism. We have previously reported that canine distemper virus (CDV) targets certain mouse brain structures, including the hypothalamus, early and selectively. Infected mice exhibit acute encephalitis, with late disease, characterized by motor impairment or obesity syndrome, appearing in some of the surviving mice several months after the initial viral replication. In the present study, we show viral persistence in the hypothalami of obese mice, as demonstrated by low, but still significant, levels of CDV nucleoprotein transcripts, associated with a dramatic decrease in F gene mRNAs. Given the pivotal role of the hypothalamus in obesity (eating behavior, energy consumption, and neuroendocrine function) and that of leptin, the adipose tissue-derived satiety factor acting through hypothalamic receptors, we analyzed the leptin networks in both obese and nonobese mice. The discrepancy found between the chronic and dramatic increase in blood leptin levels and the occurrence of obesity may be due to leptin resistance in the brain. In fact, expression of the long leptin receptor isoform, representing the functional leptin receptor, was specifically downregulated in the hypothalami of obese mice, explaining their inability to generate an adequate response to leptin in the brain. Intriguingly, during the acute phase of infection, its expression was increased in CDV-targeted structures in all infected mice and remained high in obese mice in all CDV-targeted structures, except for the hypothalamus. The biphasic change in hypothalamic leptin receptor expression seen during the progression of CDV-induced obesity provides a new paradigm for understanding mechanisms of neuroendocrinological, virus-induced abnormalities. (+info
Bone amyloidoma in a diabetic patient with morbid obesity.
Bone localisations of amyloidosis are rare, usually diffuse and associated with myeloma. We report the case of a patient with massive obesity complicated by diabetes, hypertension, sleep apnea and liver steatosis, who complained of rapidly worsening bilateral polyradiculalgia of the lower limbs. After sufficient weight loss made nuclear magnetic resonance imaging feasible, a spinal tumour was visualised on the 5th lumbar vertebra, extending to soft tissues. Total excision was performed, and pathological studies revealed an amyloid bone tumour with no evidence of myeloma. (+info
Laparoscopic Roux-en-Y gastric bypass for morbid obesity.
Surgery is currently the only effective treatment for morbid obesity. The two most commonly accepted operations are the Roux-en-Y gastric bypass and vertical banded gastroplasty. Although multiple authors have reported on a laparoscopic approach to gastric banding, the Roux-en-Y gastric bypass is a complex operation to be replicated using laparoscopic techniques. In this article, we describe our technique of the Roux-en-Y gastric bypass using a laparoscopic approach in four cases. (+info