Obese individuals have an increased preference for high caloric foods, such as sweets and fats. However, following gastric bypass (GBP) surgery, morbidly obese patients tend to avoid these foods. We hypothesize that this aversion may occur, in part, from permutations in taste acuity. To test this hypothesis, taste detection and recognition thresholds for the four basic tastes (salt, sweet, sour, and bitter) were assessed using a modification of the Henkin forced choice three stimulus technique. Taste acuity measurements were obtained at baseline and at 30, 60, and 90 days post-operative for six morbidly obese GBP women and ten non-surgical, lean female controls. We found nonsignificant differences in taste detection and recognition thresholds between morbidly obese and lean control study subjects at baseline, and no significant correlation between taste acuity and body size. Furthermore, in our study population of lean and obese women, ages 26 to 52, there were no significant interrelationships between baseline taste thresholds and known effectors of taste acuity, i.e., zinc levels, glycemic status, liver and kidney function, or age. Following GBP surgery, a significant up-regulation in taste acuity for bitter and sour was observed along with a trend toward a reduction in salt and sweet detection and recognition thresholds. These findings would suggest the following: (1) taste acuity does not influence taste preferences of the obese individual who has not had bariatric surgery; (2) taste effectors such as zinc, when within the range of normal values, do not alter thresholds of the 4 basic tastes; and (3) weight loss following gastric bypass surgery is associated with an up-regulation in taste acuity in the morbidly obese. Studies are currently under investigation at our center to identify the specific etiology of taste acuity upregulation in the morbidly obese following GBP surgery.

Although vitamin D deficiency has been well-documented following gastric bypass surgery, there are few studies of vitamin D status in the non-operative morbidly obese patient. We examined 25-hydroxyvitamin D (25-OHD) levels in 60 morbidly obese pre-operative females; 62% of them had 25-OHD levels below normal range (16-74 ng/ml) which were not associated with reductions in serum calcium or phosphorus, liver or kidney dysfunction, and were not significantly correlated to patients' age. However, 25-OHD levels were significantly (p < 0.0001) and negatively correlated to body mass (r = -0.49). These data suggest that low vitamin D may be associated with obesity per se. Hypovitaminosis D, when it is found in post-bariatric surgery patients, may not be caused by the surgery since it may have been present to some degree pre-operatively.

The prevalence of mutations within and in the flanking regions of the gene encoding the melanocortin 4 receptor was investigated in severely obese and normal-weight subjects from the Swedish Obese Subjects study, the Health, Risk Factors, Exercise Training, and Genetics (HERITAGE) Family study, and a Memphis cohort. A total of 433 white and 95 black subjects (94% females) were screened for mutations by direct sequencing. Three previously described missense variants and nine novel (three missense, six silent) variants were detected. None of them showed significant association with obesity or related phenotypes. In addition, two novel deletions were found in two heterozygous obese women: a -65_-64delTG mutation within the 5' noncoding region and a 171delC frameshift mutation predicted to result in a truncated nonfunctional receptor. No pathogenic mutations were found among obese blacks or nonobese controls. Furthermore, none of the null mutations found in other populations was present in this sample. In conclusion, our results do not support the prevailing notion that sequence variation in the melanocortin 4 receptor gene is a frequent cause of human obesity.

The morbidly obese have a disproportionately greater risk of hypertension, diabetes, and coronary artery disease than their lean or less seriously obese counterparts. Roux-en-Y gastric bypass surgery has been found to be highly effective in inducing, and sustaining, weight loss in individuals with morbid obesity. The purpose of the present study was to examine the effects of weight loss with Roux-en-Y gastric bypass surgery (GBP) on blood pressure, fasting blood glucose, and the lipid/lipoprotein status of 61 morbidly obese women and 21 men. Anthropometric and blood pressure assessments and blood samples for glucose and lipid/lipoprotein analyses were obtained before surgery and at 6 to 12 months postoperatively. By this time, morbidly obese (MO) males and females had lost 33% and 30% of their initial body weight, respectively, along with significant reductions in fasting blood glucose (p < 0.01) and systemic blood pressure (p < 0.05). Weight loss with GBP was also associated with significant reductions in the apoprotein B-containing lipoproteins and the triglyceride and cholesterol composition of these particles. There was a trend (p < 0.10) toward increased serum levels of high density lipoprotein (HDL)-cholesterol following GBP, and significant (p < 0.05) improvement in HDL subfraction distribution and composition. These findings demonstrate the effectiveness of GBP in inducing metabolic changes in the MO population, which may reduce the risk of coronary artery disease, diabetes, and hypertension.

Epidemic louse borne typhus has historically caused massive mortality in the wake of war, famine, and great migrations.1 In the four years from 1918 in Eastern Europe and Russia there were up to 30 million cases, and three million deaths. In the recent past in Burundi typhus has infected prison inmates before spreading to the wider community.2 It remains a risk among refugee populations in all parts of the world, despite its omission from a recent review of health care in refugee camps.3

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The objective of this study was to determine the molecular bases of disordered hepatic function and disease susceptibility in obesity. We compared global gene expression in liver biopsies from morbidly obese (MO) women undergoing gastric bypass (GBP) surgery with that of women undergoing ventral hernia repair who had experienced massive weight loss (MWL) following prior GBP. Metabolic and hormonal profiles were examined in MO vs. MWL groups. Additionally, we analyzed individual profiles of hepatic gene expression in liver biopsy specimens obtained from MO and MWL subjects. All patients underwent preoperative metabolic profiling. RNAs were extracted from wedge biopsies of livers from MO and MWL subjects, and analysis of mRNA expression was carried out using Affymetrix HG‐U133A microarray gene chips. Genes exhibiting greater than twofold differential expression between MO and MWL subjects were organized according to gene ontology and hierarchical clustering, and expression of key genes exhibiting differential regulation was quantified by real‐time–polymerase chain reaction (RT‐PCR). We discovered 154 genes to be differentially expressed in livers of MWL and MO subjects. A total of 28 candidate disease susceptibility genes were identified that encoded proteins regulating lipid and energy homeostasis (PLIN, ENO3, ELOVL2, APOF, LEPR, IGFBP1, DDIT4), signal transduction (MAP2K6, SOCS‐2), postinflammatory tissue repair (HLA‐DQB1, SPP1, P4HA1, LUM), bile acid transport (SULT2A, ABCB11), and metabolism of xenobiotics (GSTT2, CYP1A1). Using gene expression profiling, we have identified novel candidate disease susceptibility genes whose expression is altered in livers of MO subjects. The significance of altered expression of these genes to obesity‐related disease is discussed.

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