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PubMed1996

Restoration of growth hormone (GH) response to GH-releasing hormone in elderly and obese subjects by acute pharmacological reduction of plasma free fatty acids.

GH induces lipolysis in vivo, increasing plasma free fatty acid (FFA) levels; in turn, FFA are able to reduce GH release, and acipimox, a nicotinic acid analog able to block lipolysis, enhances in normal subjects the GH response to GHRH. Obesity and old age are characterized by a blunted GH response to several stimuli, including GHRH; reports also indicate high plasma FFA levels in obesity and sometimes in the elderly. The aim of this study was to evaluate the possible role of FFA in GH release in obese and elderly subjects. According to a randomized, single blind, cross-over protocol, six healthy subjects, six obese subjects, and six elderly subjects received on 2 different days, with a 1-week interval, placebo or acipimox (250 mg, orally) at 0700 and 1100 h; GHRH [GHRH-(1-44)NH2; 50 micrograms in healthy subjects and in elderly subjects, 100 micrograms in obese subjects] was injected iv at 1300 h, and blood samples for evaluation of plasma FFA, blood glucose, serum insulin (IRI), and serum GH levels were taken from 1200 to 1500 h. Plasma FFA levels were always lower (P < 0.05) after acipimox than after placebo (0.03 +/- 0.01 vs. 0.13 +/- 0.02 g/L in healthy subjects, 0.09 +/- 0.01 vs. 0.27 +/- 0.02 g/L in obese, 0.02 +/- 0.005 vs. 0.17 +/- 0.01 g/L in elderly subjects); serum IRI levels were also lower (P < 0.05) after acipimox than after placebo in the three groups of subjects (16 +/- 3 vs. 30 +/- 5, 120 +/- 30 vs. 181 +/- 32, and 21 +/- 3 vs. 49 +/- 9 pmol/L); both FFA (P < 0.05) and IRI levels (P < 0.05) were higher in obese than in healthy or elderly subjects after placebo and acipimox. Blood glucose levels were not different in the three groups of subjects after either placebo or acipimox. The integrated GH response to GHRH-(GH delta area) was always greater (P < 0.05) after acipimox than after placebo (4677 +/- 633 vs. 1599 +/- 373 in healthy, 1469 +/- 230 vs. 343 +/- 114 in obese, 2304 +/- 759 vs. 325 +/- 133 micrograms/L.120 min in elderly subjects); after both placebo and acipimox, the GH delta area was greater (P < 0.05) in healthy subjects than in obese or elderly subjects. The GH delta area of elderly and obese subjects after acipimox was not different from the GH delta area of healthy subjects after placebo. Changes in GH delta areas were not significantly related to changes in FFA or IRI induced by acipimox; in contrast, absolute values of FFA and IRI as well as basal GH levels were all significantly related to the GH delta area. At multiple regression analysis, FFA was the only significant predictor of GH delta area. These data indicate that acute pharmacological reduction of plasma FFA levels restores the blunted GH response to GHRH commonly observed in obese and elderly subjects: however, when lipolysis is blocked to a similar extent, healthy subjects still show a higher GH delta area than obese or elderly subjects. As FFA are the best predictor of the GH delta area, we suggest that in obesity, the blunted GH release is due to high FFA levels, whereas in the elderly there might be an abnormal sensitivity to normal FFA levels.

Adult↗
PubMed2005

Public opinion and the politics of obesity in America.

Health policy experts have recently sounded the warning about the severe health and economic consequences of America's growing rates of obesity. Despite this fact, obesity has only begun to enter America's political consciousness and we have little information about what average Americans think of obesity or whether they support obesity-related policies. Using unique survey data collected by the authors, this essay examines public attitudes toward obesity and obesity policy. We find that, contrary to the views of health experts, most Americans are not seriously concerned with obesity, express relatively low support for obesity-targeted policies, and still view obesity as resulting from individual failure rather than environmental or genetic sources. Given the absence of elite discourse on this problem, we also find that typical determinants of policy preferences, such as ideology or partisanship, are not good predictors of attitudes on obesity policy. Rather, with a low-valence issue such as obesity, the public utilizes other attitudinal frameworks such as their opinions on smoking policy and the environmental culpability for obesity. The implications of these findings for obesity policy and research on health-related public opinion are discussed.

Attitude to Health↗
PubMed2006

Treating child obesity and associated medical conditions.

With American children on course to grow into the most obese generation of adults in history, Sonia Caprio argues that it is critical to develop more effective strategies for preventing childhood obesity and treating serious obesity-related health complications. She notes that although pediatricians are concerned about the obesity problem, most are ineffective in addressing it. Treatment should begin, Caprio explains, with a thorough medical exam, an assessment of nutrition and physical activity, an appraisal of the degree of obesity and associated health complications, a family history, and full information about current medications. Caprio also summarizes the current use of medications and surgery in treating child obesity and argues, that for severe forms of obesity, the future lies in developing new and more effective drugs. Caprio explains that today's most effective obesity treatment programs have been carried out in academic centers through an approach that combines a dietary component, behavioral modification, physical activity, and parental involvement. Such programs, however, have yet to be translated to primary pediatric care centers. Successfully treating obesity, she argues, will require a major shift in pediatric care that builds on the findings of these academic centers regarding structured intervention programs. To ensure that pediatricians are well trained in implementing such programs, the American Medical Association is working with federal agencies, medical specialty societies, and public health organizations to teach doctors how to prevent and manage obesity in both children and adults. Such training should be a part of undergraduate and graduate medical education and of continuing medical education programs. Caprio also addresses the problem of reimbursement for obesity treatment. Despite the health risks of obesity, patients get little support from health insurers, thus putting long-term weight-management programs beyond the reach of most. Caprio argues that obesity should be recognized as a disease and receive coverage for its treatment just as other diseases do.

Child↗
PubMed2006

The consequences of childhood overweight and obesity.

Researchers are only gradually becoming aware of the gravity of the risk that overweight and obesity pose for children's health. In this article Stephen Daniels documents the heavy toll that the obesity epidemic is taking on the health of the nation's children. He discusses both the immediate risks associated with childhood obesity and the longer-term risk that obese children and adolescents will become obese adults and suffer other health problems as a result. Daniels notes that many obesity-related health conditions once thought applicable only to adults are now being seen in children and with increasing frequency. Examples include high blood pressure, early symptoms of hardening of the arteries, type 2 diabetes, nonalcoholic fatty liver disease, polycystic ovary disorder, and disordered breathing during sleep. He systematically surveys the body's systems, showing how obesity in adulthood can damage each and how childhood obesity exacerbates the damage. He explains that obesity can harm the cardiovascular system and that being overweight during childhood can accelerate the development of heart disease. The processes that lead to a heart attack or stroke start in childhood and often take decades to progress to the point of overt disease. Obesity in childhood, adolescence, and young adulthood may accelerate these processes. Daniels shows how much the same generalization applies to other obesity-related disorders-metabolic, digestive, respiratory, skeletal, and psychosocial-that are appearing in children either for the first time or with greater severity or prevalence. Daniels notes that the possibility has even been raised that the increasing prevalence and severity of childhood obesity may reverse the modern era's steady increase in life expectancy, with today's youth on average living less healthy and ultimately shorter lives than their parents-the first such reversal in lifespan in modern history. Such a possibility, he concludes, makes obesity in children an issue of utmost public health concern.

Cardiovascular Diseases↗
PubMed2005

Gallbladder pathology in morbid obesity.

BACKGROUND: Obese patients are at increased risk for biliary disease. The prevalence and type of gallbladder pathology in morbidly obese patients was evaluated, and compared with a non-obese control group. METHODS: A consecutive series of obese patients (n=478) who had undergone bariatric surgery with concurrent routine cholecystectomy and a consecutive group of organ donors (n=481) were compared. Gallbladder pathology was defined as: cholelithiasis, cholecystitis, cholesterolosis, or normal pathology. RESULTS: Mean age of obese patients and of donors was 42 +/- 9 and 43 +/- 17 years respectively and mean BMI was 52 +/- 10 and 27 +/- 7 kg/m2 respectively, P<0.05. There were more females in the obesity group (88% vs 47%, P<0.0001). 31% of obese patients and 7% of controls had a previous cholecystectomy (P<0.0001). 21% of the obese and 72% of the controls had normal gallbladder pathology (P<0.0001). Overall, obese patients had a higher incidence of cholelithiasis (25% vs 5%, P<0.0001), cholecystitis (50% vs 17%, P<0.0001), and cholesterolosis (38% vs 6%, P<0.0001) compared with controls. Obese patients with BMI <50 were more likely than those with BMI > or =50 to have normal gallbladder pathology (27% vs 14%, P<0.001). Female patients were more likely to have undergone previous cholecystectomy than males in both the obese group (34% vs 11%, P<0.001) and the control group (12% vs 2%, P<0.0001). Normal pathology was more common in male patients (80% vs 63%, P<0.0001) and patients <50 years (76% vs 66%, P<0.05) in the control group. CONCLUSIONS: Obese patients have an increased incidence of benign gallbladder disease than a group of controls, and the relative risk appears to be positively correlated with the level of increase in the BMI. Obesity appears to change the effect of age and gender on gallbladder pathology.

Adolescent↗
PubMedDate not supplied

Obesity and lipid profiles in children and adolescents.

Childhood obesity is associated with unfavorable lipid profile, suggesting that obese children should be screened for hypercholesterolemia. However, the prevalence of hypercholesterolemia in childhood obesity, and the effect of the degree of obesity on lipid profile, are unknown. Eighty-nine obese children and adolescents (BMI >85%, mean age 10.4 +/- 2.5 years) and 53 non-obese control children matched for age, gender and pubertal stage participated in the study. Early morning blood samples for serum lipids were collected in all children after a 12-h fast. Mean serum cholesterol and triglycerides (TG) levels were significantly higher (p <0.05) among the obese children (cholesterol: 175.2 +/- 31.4 vs 143.3 +/- 24.3 mg/dl; TG: 122.8 +/- 69.7 vs 94.3 +/- 37.8 mg/dl in obese and control children, respectively). Among the obese children, 52% had elevated serum cholesterol levels (>170 mg/dl) compared to 16% in the controls. The degree of obesity (BMI 85-95% vs BMI >95%) had no effect on serum lipids. Unfavorable lipid levels were relatively common among obese children, suggesting that obesity should be considered a risk factor for hypercholesterolemia, and that screening obese children for hypercholesterolemia should be considered.

Adolescent↗
PubMed2005

Increased prevalence of obesity in children with functional constipation evaluated in an academic medical center.

OBJECTIVE: The rapidly increasing prevalence of obesity in children is the most important problem facing pediatricians today. A recent study suggested an association of obesity and constipation in children but lacked a control group for comparison. The objectives of this study were to evaluate the prevalence of obesity in a large cohort of children with functional constipation and to compare it with a control group representative of the general population. METHODS: Retrospective chart review was performed on 719 children, between the ages of 4 and <18 years, with chronic functional constipation seen in the general pediatric and pediatric gastroenterology clinics between July 2002 and June 2004. Data collected included age, gender, BMI, and signs and symptoms of constipation including fecal incontinence. Obesity was classified as a BMI of >95th percentile and severe obesity as a BMI of > or =5 kg/m2 above the 95th percentile for age and gender. The control group consisted of all 930 children (4 to <18 years of age) presenting to the pediatric clinic for a well-child visit between January and June 2004. The chi2 and t tests were used for analysis. RESULTS: Overall prevalence of obesity was significantly higher in constipated children (22.4%) compared with control children (11.7%), and this higher prevalence was also seen for severe obesity. The prevalence rates of obesity were significantly higher in constipated males (25%) than in constipated females (19%) and were significantly higher compared with the control males (13.5%) and control females (9.8%). Constipated boys in all 3 age groups had significantly higher rates of obesity than the control boys; the constipated girls had significantly higher obesity rates for the age groups between 8 and <18 years. Fecal incontinence (encopresis) was present in 334 of 719 (46%) constipated children. The prevalence of obesity was similar in constipated children with and without fecal incontinence. CONCLUSIONS: There is a significantly higher prevalence of obesity in children with constipation compared with age- and gender-matched controls. This higher prevalence is present in both boys (4 to <18 years of age) and girls (8 to <18 years of age) with constipation and is not related to the presence of fecal incontinence among constipated children. The higher prevalence of obesity may be a result of dietary factors, activity level, or hormonal influences and needs additional evaluation.

Adolescent↗
PubMed2000

Endocrine, metabolic and cardioprotective effects of hexarelin in obese Zucker rats.

Genetically obese male Zucker rats have an impaired secretion of GH, coupled to hyperinsulinemia, hyperlipidemia and glucose intolerance. The aim of this study was to evaluate whether a chronic treatment with hexarelin, a synthetic enkephalin-derived hexapeptide with a potent GH-releasing activity, might be able to ameliorate the somatotropic function and reverse some metabolic alterations associated with obesity in male obese Zucker rats. Furthermore, as decreased GH secretion and insulin resistance are associated with increased cardiovascular risk, we also tested the capacity of hexarelin to prevent postischemic ventricular dysfunction in hearts of male obese Zucker rats. Obese and lean male rats of the Zucker strain were treated with hexarelin (80 microgram/kg, b.i.d., s.c.) or saline (1 ml/kg, b.i.d., s.c.) for 30 days. An acute hexarelin injection (80 microgram, s.c.) at the 28th day of treatment elicited a rise in plasma GH levels in ! lean but not in obese rats (pretreated or not with hexarelin); lean rats chronically treated with hexarelin showed a greater increase in plasma GH as compared with control counterparts. At the end of the experiment, pituitary GH mRNA levels were significantly reduced in obese rats and hexarelin administration failed to increase pituitary GH mRNA and IGF-I concentrations in plasma and heart. Chronic treatment with hexarelin increased insulinemia and blood glucose levels in obese but not in lean rats, left unaltered the high triglyceride levels but significantly decreased plasma cholesterol concentrations in obese rats. Heart preparations from lean and obese Zucker rats treated with saline, subjected to low flow ischemia and reperfusion, showed at reperfusion: a) a low recovery of postischemic left ventricular developed pressure (LVDP), coupled to a substantial increase in coronary perfusion pressure, and b) a marked increase in creatine kinase released in the perfusates. Hexare! lin administration for 30 days counteracted the heart ischemic damage both in lean and obese Zucker rats. In fact, the recovery of LVDP at reperfusion was significantly higher than in controls and the increase in coronary resistance was minimal. Collectively, these data indicate that a 30-day treatment with hexarelin was unable to improve somatotropic function in male obese Zucker rats but was successful in decreasing plasma cholesterol concentrations. Hexarelin exerted a cardioprotective effect in both lean and obese rats. The heart-protective activity afforded by the peptide was divorced from any stimulation of the GH axis and is probably exerted through activation of specific cardiac receptors.

6-Ketoprostaglandin F1 alpha↗
PubMed2002

Genetics of obesity.

Obesity is a typical common multifactorial disease in which environmental and genetic factors interact. In rare cases of severe obesity with childhood onset, a single gene has a major effect in determining the occurrence of obesity, with the environment having only a permissive role in the severity of the phenotype. Exceptional mutations of the leptin gene and its receptor, pro-opiomelanocortine (POMC), prohormone convertase 1 (PC1) and more frequently, mutations in the melanocortin receptor 4 (1 to 4% of very obese cases) have been described. All these obesity genes encode proteins that are strongly connected as part of the same loop of the regulation of food intake. They all involve the leptin axis and one of its hypothalamic targets; the melanocortin pathway. Pathways of bodyweight regulation involved in monogenic forms of obesity might represent targets for future drug development. Successful leptin protein replacement in a leptin-deficient child has contributed to the validation of the usefulness of gene screening in humans. However, the individual variability in response to leptin treatment might be related to genetic variability. The efficiency of leptin itself or of small-molecule agonists of the leptin receptor should be studied in relation with genetic variations in the leptin gene promoter. The most common forms of obesity are polygenic. Two general approaches have been used to date in the search for genes underlying common polygenic obesity in humans. The first approach focuses on selected genes having some plausible role in obesity on the basis of their known or presumed biological role. This approach yielded putative susceptibility genes with only small or uncertain effects. The second approach attempts to map genes purely by position and requires no presumptions on the function of genes. Genome-wide scans identify chromosomal regions showing linkage with obesity in large collections of nuclear families. Genome-wide scans in different ethnic populations have localized major obesity loci on chromosomes 2, 5, 10, 11 and 20. Susceptibility gene(s) for obesity may be positionally cloned in the intervals of linkage. The candidate gene and positional cloning of major obesity-linked regions approaches are discussed in this paper.

Genetic Linkage↗
PubMed1995

Diabetic ketoacidosis in obese African-Americans.

Our preliminary data indicate that 15% of African-American patients presenting with diabetic ketoacidosis (DKA) are obese. To determine underlying mechanisms, we analyzed the clinical characteristics and indexes of insulin secretion and insulin sensitivity in 35 obese patients with DKA, 22 obese patients with hyperglycemia, 10 lean patients with DKA, and 10 obese nondiabetic subjects. Studies were performed 1 day after resolution of DKA and after 12 weeks of follow-up. At presentation, both obese DKA and obese hyperglycemic patients had no detectable insulin response to intravenous glucose, but they did respond to glucagon administration. The acute insulin response (AIR) to glucagon in obese DKA patients (0.9 +/- 0.1 ng/ml, P < 0.01), but significantly greater than in lean patients with DKA (0.1 +/- 0.1 ng/ml, P < 0.01). After 12 weeks of follow-up, the AIR to glucose improved in both groups of obese diabetic patients but remained significantly lower than in nondiabetic control subjects (both P < 0.01). In contrast, the AIR to glucagon was not significantly different from that in obese control subjects. Insulin sensitivity was decreased in both groups of obese diabetic patients at presentation and improved after follow-up to levels similar to those in obese nondiabetic control subjects. Reactivity with islet cell antibodies was not detected in any of the patients. During follow-up, 25 of 35 obese DKA and 16 of 22 hyperglycemic patients were able to discontinue insulin therapy, with continued good metabolic control. Our results indicate that in African-Americans, obese patients with DKA represent a subset of type II diabetes.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Effect of obesity on insulin resistance in normal subjects and patients with NIDDM.

Insulin resistance (IR) is a characteristic feature of non-insulin-dependent diabetes mellitus (NIDDM) as well as obesity, and a majority of NIDDM patients are obese. To assess the effect of obesity independent of NIDDM on IR, we studied the relationship between IR and obesity in 65 normal and 58 NIDDM subjects; we used body mass index (BMI) as a measure of obesity and glucose infusion rate (GINF) during a euglycemic hyperinsulinemic (120 mU.m-2.min-1) glucose clamp as a measure of IR. In lean normal subjects, GINF was 57.7 +/- 2.2 mumol.kg-1.min-1 (10.4 +/- 0.4 mg.kg-1.min-1) and the lean NIDDM subjects were markedly insulin-resistant, with a GINF of 34.4 +/- 2.8 mumol.kg-1.min-1 (6.2 +/- 0.5 mg.kg-1.min-1). Obese normal subjects were also insulin-resistant compared with lean normal subjects, with a GINF of 36.1 +/- 2.2 mumol.kg-1.min-1 (6.5 +/- 0.4 mg.kg-1.min-1), and obesity caused an increase in IR in NIDDM, with a GINF of 21.1 +/- 1.4 mumol.kg-1.min-1 (3.8 +/- 0.25 mg.kg-1.min-1) in the obese NIDDM subjects. Therefore, approximately 61% of the IR in obese NIDDM subjects is due to NIDDM, with 39% due to obesity, demonstrating a greater impact of NIDDM than of obesity in causing IR. The correlation between GINF and BMI was much better in normal subjects (r = -0.75) than in NIDDM subjects (r = -0.50) as was the relationship between fasting insulin level and BMI (r = -0.59 in normal subjects, r = -0.48 in NIDDM subjects). As expected, the fasting insulin level was also strongly correlated to GINF in normal subjects (r = -0.61); however, this relationship was weaker in NIDDM subjects ( r = -0.46). In conclusion, 1) obesity has a major impact to cause insulin resistance in nondiabetic subjects, but the effect of obesity on IR in NIDDM is less; 2) NIDDM per se is the major contributor to IR in NIDDM; and 3) the fasting insulin level is a better surrogate marker of IR in nondiabetic subjects than in NIDDM patients.

Adult↗
PubMed2005

Inducible nitric oxide synthase has divergent effects on vascular and metabolic function in obesity.

Previous studies have suggested an involvement of inducible nitric oxide synthase (iNOS) in obesity, but the relation, if any, between this and mechanisms underlying endothelial dysfunction in obesity is unknown. We studied mice fed an obesogenic high-fat or standard diet for up to 8 weeks. Obesity was associated with elevated blood pressure; resistance to the glucoregulatory actions of insulin; resistance to the vascular actions of insulin, assessed as the reduction in phenylephrine constrictor response of aortic rings after insulin preincubation (lean -21.7 +/- 11.5 vs. obese 18.2 +/- 15.5%; P < 0.05); and evidence of reactive oxygen species (ROS)-dependent vasodilatation in response to acetylcholine in aortic rings (change in maximal relaxation to acetylcholine after exposure to catalase: lean -2.1 +/- 6.0 vs. obese -15.0 +/- 3.8%; P = 0.04). Obese mice had increased expression of iNOS in aorta, with evidence of increased vascular NO production, assessed as the increase in maximal constriction to phenylephrine after iNOS inhibition with 1400W (lean -3.5 +/- 9.1 vs. obese 42.1 +/- 11.2%; P < 0.001). To further address the role of iNOS in obesity-induced vascular and metabolic dysfunction, we studied the effect of a high-fat diet in iNOS knockout mice (iNOS KO). Obese iNOS KO mice were protected against the development of resistance to insulin's glucoregulatory and vascular effects (insulin-dependent reduction in maximal phenylephrine response: obese wild-type 11.2 +/- 15.0 vs. obese iNOS KO -20.0 +/- 7.7%; P = 0.02). However, obese iNOS KO mice remained hypertensive (124.0 +/- 0.7 vs. 114.9 +/- 0.5 mmHg; P < 0.01) and had evidence of increased vascular ROS production. Although these data support iNOS as a target to protect against the adverse effects of obesity on glucoregulation and vascular insulin resistance, iNOS inhibition does not prevent the development of raised blood pressure or oxidative stress.

Acetylcholine↗
PubMed2003

Effects of obesity on lipid profiles in neutered male and female cats.

OBJECTIVE: To examine whether obese cats, compared with lean cats, have alterations in lipoprotein metabolism that might lead to a decrease in glucose metabolism and insulin secretion. ANIMALS: 10 lean and 10 obese adults cats (5 neutered males and 5 neutered females each). PROCEDURE: Intravenous glucose tolerance tests with measurements of serum glucose, insulin, and nonesterified fatty acid (NEFA) concentrations were performed. Lipoprotein fractions were examined in serum by isopycnic density gradient ultracentrifugation. RESULTS: Obese cats had insulin resistance. Plasma triglyceride and cholesterol concentrations were significantly increased in obese cats, compared with lean cats. Very low density lipoprotein (VLDL) concentrations were increased in obese cats, compared with lean cats; however, the composition of various fractions remained unchanged between obese and lean cats, indicating greater synthesis and catabolism of VLDL in obese cats. Serum high density lipoprotein (HDL) cholesterol concentrations were increased in obese cats, compared with lean cats. Serum NEFA concentrations were only significantly different between obese and lean cats when separated by sex; obese male cats had higher baseline serum NEFA concentrations and greater NEFA suppression in response to insulin, compared with lean male cats. CONCLUSIONS AND CLINICAL RELEVANCE: Lipid metabolism changes in obese cats, compared with lean cats. The increase in VLDL turnover in obese cats might contribute to insulin resistance of glucose metabolism, whereas the increase in serum HDL cholesterol concentration might reflect a protective effect against atherosclerosis in obese cats.

Animals↗
PubMedDate not supplied

Underdiagnosis of obesity at a community health center.

BACKGROUND: Obesity is at epidemic proportions. This study examined the extent to which obesity is being diagnosed at a community health center residency-training site. Results were examined by provider type. Characteristics of patients with obesity diagnosed by primary care providers were compared with characteristics of patients determined to be obese by body mass index (BMI) calculation exclusively. METHODS: A cross-sectional design was used. Medical records of 465 adult patients were audited. Data collected included diagnosis of obesity, height and weight, demographics, and comorbidity. RESULTS: Of the 465 patients' charts audited, 83 contained a provider diagnosis of obesity, and 74 additional patients were determined to be obese by BMI calculation exclusively. Significant underdiagnosis occurred among all provider types (P = .036). Patients with a diagnosis of obesity had significantly higher BMI scores (38.4 vs 34.4, P = .002). Obesity was more likely to be diagnosed in female than in male patients (P = .001). Differences related to age, insurance coverage, and comorbidity were not significant. CONCLUSIONS: Obesity was found to be an underdiagnosed condition among all provider types. As evidenced by significantly higher BMI scores for provider-diagnosed obesity, the data suggest that the obesity diagnosis is made by appearance. The importance of teaching and modeling the use of BMI to diagnose obesity is underscored.

Adolescent↗
PubMed2004

Are mood disorders and obesity related? A review for the mental health professional.

OBJECTIVE: We reviewed evidence regarding a possible relationship between mood disorders and obesity to better inform mental health professionals about their overlap. METHOD: We performed a MEDLINE search of the English-language literature for the years 1966-2003 using the following terms: obesity, overweight, abdominal, central, metabolic syndrome, depression, mania, bipolar disorder, binge eating, morbidity, mortality, cardiovascular, diabetes, cortisol, hypertriglyceridemia, sympathetic, family history, stimulant, sibutramine, antiobesity, antidepressant, topiramate, and zonisamide. We evaluated studies of obesity (and related conditions) in persons with mood disorders and of mood disorders in persons with obesity. We also compared studies of obesity and mood disorders regarding phenomenology, comorbidity, family history, biology, and pharmacologic treatment response. RESULTS: The most rigorous clinical studies suggest that (1). children and adolescents with major depressive disorder may be at increased risk for developing overweight; (2). patients with bipolar disorder may have elevated rates of overweight, obesity, and abdominal obesity; and (3). obese persons seeking weight-loss treatment may have elevated rates of depressive and bipolar disorders. The most rigorous community studies suggest that (1). depression with atypical symptoms in females is significantly more likely to be associated with overweight than depression with typical symptoms; (2). obesity is associated with major depressive disorder in females; and (3). abdominal obesity may be associated with depressive symptoms in females and males; but (4). most overweight and obese persons in the community do not have mood disorders. Studies of phenomenology, comorbidity, family history, biology, and pharmacologic treatment response of mood disorders and obesity show that both conditions share many similarities along all of these indices. CONCLUSION: Although the overlap between mood disorders and obesity may be coincidental, it suggests the two conditions may be related. Clinical and theoretical implications of this overlap are discussed, and further research is called for.

Adolescent↗
PubMed2003

Decreased plasma adiponectin levels in young obese males.

Plasma adiponectin levels are reduced in middle-aged obesity and in patients with type 2 diabetes and coronary artery disease. The purpose of this study was to investigate the effects of early-aged obesity on plasma adiponectin level. Twenty-six male college students (19.2 +/- 1.1 years, obese group: n = 15, [body mass index > 25, percent body fat > 25%], non-obese group: n = 11) participated in the present study. We measured anthropometric parameters and plasma adiponectin and leptin level. Plasma adiponectin levels in the obese group were significantly lower than those in the non-obese group (obese: 4.7 +/- 2.0 micro g/ml, non-obese: 6.8 +/- 2.2 micro g/ml, p < 0.05). On the other hand, plasma leptin levels in the obese group were significantly higher than those in the non-obese group (obese: 8.4 +/- 3.2 ng/ml, non-obese: 2.6 +/- 2.1 ng/ml, p < 0.001). Plasma adiponectin levels were significantly correlated with body weight (r = -0.415, p < 0.05) and percent body fat (r = -0.412, p < 0.05). Stepwise multiple regression analysis revealed that percent body fat was a significant independent predictor of plasma adiponectin level (r = 0.406, p < 0.05). These results show that obesity is associated with reduced plasma adiponectin even in young subjects.

Adiponectin↗
PubMed2000

Diffuse idiopathic skeletal hyperostosis in diabetes mellitus, impaired glucose tolerance and obesity.

BACKGROUND: Diffuse idiopathic skeletal hyperostosis (DISH) is a rheumatic disease characterized by a significant association with metabolic alterations, such as an impaired lipidic profile. METHODS: One-hundred-thirty consecutive patients and 40 normal subjects were studied. The patients were affected by type 1 and type 2 diabetes mellitus, impaired glucose tolerance and obesity. The diagnosis of DISH was performed by clinical examination and X-ray study of the thoracolumbar spine. The determination of total cholesterol, triglycerides, HLD-cholesterol and LDL-cholesterol was realized by routine biochemical methods; an oral glucose tolerance test was performed in order to determine the levels of C-peptide and blood glucose. RESULTS: We demonstrate a high incidence of the disease in a cohort of patients affected by overt and non-overt diabetes mellitus (T1DM and T2DM) as well as in obese subjects and a correlation between this disorder and hypertryglyceridemia (T1DM, obese-T2DM and obese patients), hypo-HDL-cholesterolemia (obese-T2DM, non-obese-T2DM and obese patients) and hyper-LDL-cholesterolemia (obese patients). In obese-T2DM patients, as well as in obese patients, we observed 40% of DISH, in non obese-T2DM patients the presence of DISH was 30%, while in T1DM patients and impaired glucose tolerance 26.6% and 22.2, respectively. However, a correlation between DISH and the relative hyperinsulinemia in obese patients during an oral glucose tolerance test is not documented. CONCLUSIONS: Our study confirms the prevalence of DISH in diabetes mellitus and obesity, the association with an impaired lipidic profile and the low percentage of symptomatic patients.

Adult↗
PubMed1992

The effects of gonadectomy on glucose tolerance of genetically obese (fa/fa) rats: influence of sex and genetic background.

In both humans and rodents the occurrence and severity of obesity-associated non-insulin dependent diabetes mellitus (NIDDM) may be influenced by both gonadal hormones and genetic background. Early gonadectomy (at 3-5 days of age) of female and male Wistar diabetic fatty (WDF) rats and of male Zucker rats allowed us to examine these effects in genetically obese rats carrying the fatty (fa) gene. Impairment of glucose tolerance and insulin sensitivity by obesity, and amelioration or exacerbation (in the case of female rats) of this impairment by gonadectomy were assessed by intragastric glucose tolerance tests when the rats reached adulthood. Both glucose tolerance and insulin sensitivity were significantly deranged in obese WDF rats of both sexes and in obese male Zucker rats compared to lean controls of the same sex and strain. Obese male WDF rats were less glucose tolerant and insulin sensitive than were obese male Zucker rats. Glucose intolerance was not ameliorated by castration in lean or obese male WDF or Zucker rats. Insulin sensitivity was significantly improved by castration in obese male rats of both strains, as fasting plasma insulin levels and total areas under the insulin curves were significantly reduced compared to obese sham-operated controls. This effect was greater in the Zucker than in the WDF male rats. Castration significantly decreased the insulin response areas in obese male Zucker rats, but did not alter those of the obese male WDF rats. Ovariectomy did not alter glucose homeostasis of obese female WDF rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗