Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “OBESITY”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 181 records · Page 10Linked to original sources
PubMed1994

Central obesity and hypertension. Relationship between fasting serum insulin, plasma renin activity, and diastolic blood pressure in young obese subjects.

This study was designed to evaluate the role of fasting serum insulin and plasma renin activity in obesity-induced hypertension. In view of this, plasma catecholamines, fasting serum insulin (IRI), urinary sodium excretion (NaU), plasma renin activity (PRA), and plasma aldosterone (PA) levels were assessed in young (age less than 40 years) normotensive (n = 27) and hypertensive (n = 14) subjects with central obesity and in lean normotensives (n = 20). Central obesity was evaluated by waist-to-hip ratio (WHR) according to the indication of the Italian Consensus Conference of Obesity. PRA, PA, IRI, and plasma norepinephrine levels were significantly (P < .05) higher in both obese groups than in lean normotensives. PRA was significantly (P < .05) higher and NaU was significantly (P < .05) lower in obese hypertensives than in obese normotensives. Diastolic blood pressure correlated directly with WHR and PRA in normotensive and hypertensive obese subjects and with IRI but only in normotensive obese subjects. Multiple regression analysis indicated that diastolic blood pressure values increased with WHR (P < .05), IRI (P < .005), and PRA (P < .002), but not with body mass index, NaU, and norepinephrine levels. Our results indicated that increased PRA could play an important role in the development of hypertension in subjects with central obesity.

Adult↗
PubMed2004

Impaired microvascular function in obesity: implications for obesity-associated microangiopathy, hypertension, and insulin resistance.

BACKGROUND: Obesity is associated with an increased risk of developing microangiopathy, hypertension, and insulin resistance. We hypothesized that obesity is a primary cause of microvascular dysfunction, which may contribute to the development of these obesity-related disorders. METHODS AND RESULTS: We examined microvascular function in 16 lean (body mass index <24 kg/m2) and 12 obese (body mass index >30 kg/m2) healthy women (mean age, 38.9+/-6.7 years) in the basal state and during physiological systemic hyperinsulinemia. We determined skin capillary recruitment after arterial occlusion with capillaroscopy and skin endothelium-(in)dependent vasodilation by iontophoresis of acetylcholine and sodium nitroprusside. Obese women, compared with lean women, had higher systolic blood pressure (P<0.05), impaired insulin sensitivity (P<0.01), impaired capillary recruitment in the basal state (P<0.05) and during hyperinsulinemia (P<0.05), and impaired acetylcholine-mediated vasodilation in the basal state (P<0.05) and during hyperinsulinemia (P<0.01). Sodium nitroprusside-mediated vasodilation was similar in lean and obese women. Capillary recruitment and acetylcholine-mediated vasodilation were positively correlated with insulin sensitivity (r=0.58, P<0.01 and r=0.55, P<0.01, respectively) and negatively with blood pressure (r=-0.64, P<0.001 and r=-0.42, P<0.05, respectively) in both lean and obese women. CONCLUSIONS: Obesity is characterized by impaired microvascular function in the basal state and during hyperinsulinemia and, in both lean and obese women, microvascular dysfunction is associated with increased blood pressure and decreased insulin sensitivity. These findings are consistent with a contribution of impaired microvascular function to the development of obesity-related microangiopathy, hypertension, and insulin resistance.

Adult↗
PubMed2000

Role of tumor necrosis factor-alpha gene locus in obesity and obesity-associated hypertension in French Canadians.

Obesity represents a serious risk factor for the development of cardiovascular diseases, including hypertension. Segregation studies suggest that obesity and obesity-associated hypertension may share some genetic determinants. The results of the present candidate gene investigation suggest that in hypertensive pedigrees of French-Canadian origin, one such determinant is the tumor necrosis factor (TNF)-alpha gene locus. Gender-pooled quantitative sib-pair analysis demonstrated a significant effect of the gene locus on 3 global and 7 regional measures of obesity (P=0.05 to 0.0004). Gender-separate quantitative sib-pair analyses showed that the impact of the locus on obesity is most significant in the abdominal region in men and in the thigh region in women. Furthermore, the haplotype relative-risk test demonstrated a significant association between the TNF-alpha gene locus and both obesity (P=0.006) and obesity-associated hypertension (P=0.02). These effects were most significant in individuals with nonmorbid obesity. In conclusion, the results of linkage and association analyses suggest that in hypertensive pedigrees of French-Canadian origin, the TNF-alpha gene locus contributes to the determination of obesity and obesity-associated hypertension. In addition, the data indicate that gender modifies the effect of the locus on the regional distribution of body fat.

Body Mass Index↗
PubMed1983

Studies of liver insulin receptors in non-obese and obese human subjects.

The insulin-binding isotherms and the structural composition of human liver insulin receptors were examined by using plasma membranes that were prepared from liver biopsies of nine non-obese and 10 obese subjects undergoing elective surgery. The insulin-binding characteristics of liver membranes from non-obese subjects were quite similar to those previously described in rat liver membranes. However, when the membranes from obese subjects were compared with the non-obese group, insulin-binding activity was reduced by 50% (P less than 0.01). The reduction in obesity resulted primarily from a decrease in total receptor number, although a small decrease in receptor affinity was also observed. Insulin binding was not correlated with sex or with the fasting plasma insulin level. The insulin-binding sites of liver membranes were affinity-labeled with 125I-insulin and the cross-linking reagent, disuccinimidyl suberate. The liver membranes from both the non-obese and the obese group had heterogenous (nonreduced) insulin-binding species of 300,000, 260,000, and 150,000 mol wt, which were again comparable to the findings reported in rat liver. Sulfhydryl reduction demonstrated a major sub-unit of 125,000 and a minor component of 40,000-45,000 in both groups. These results indicate a close similarity between the hepatic insulin receptor of man and the more intensely studied rat hepatic receptor. Obesity in human subjects is associated with a loss of hepatic insulin receptors. This alteration may contribute to the insulin resistance reported in this organ as well as to obesity-mediated glucose tolerance.

Adult↗
PubMed1999

Cephalometric abnormalities in non-obese and obese patients with obstructive sleep apnoea.

The aim of this work was to comprehensively evaluate the cephalometric features in Japanese patients with obstructive sleep apnoea (OSA) and to elucidate the relationship between cephalometric variables and severity of apnoea. Forty-eight cephalometric variables were measured in 37 healthy males and 114 male OSA patients, who were classed into 54 non-obese (body mass index (BMI) <27 kg x m(-2), apnoea-hypopnoea index (AHI)=25.3+/-16.1 events x h(-1)) and 60 obese (BMI > or = 27 kg x m(-2), AHI=45.6+/-28.0 events h(-1)) groups. Diagnostic polysomnography was carried out in all of the OSA patients and in 19 of the normal controls. The non-obese OSA patients showed several cephalometric defects compared with their BMI-matched normal controls: 1) decreased facial A-P distance at cranial base, maxilla and mandible levels and decreased bony pharynx width; 2) enlarged tongue and inferior shift of the tongue volume; 3) enlarged soft palate; 4) inferiorly positioned hyoid bone; and 5) decreased upper airway width at four different levels. More extensive and severe soft tissue abnormalities with a few defects in craniofacial bony structures were found in the obese OSA group. For the non-obese OSA group, the stepwise regression model on AHI was significant with two bony structure variables as determinants: anterior cranial base length (S-N) and mandibular length (Me-Go). Although the regression model retained only linear distance between anterior vertebra and hyoid bone (H-VL) as an explainable determinant for AHI in the obese OSA group, H-VL was significantly correlated with soft tissue measurements such as overall tongue area (Ton), inferior tongue area (Ton2) and pharyngeal airway length (PNS-V). In conclusion, Japanese obstructive sleep apnoea patients have a series of cephalometric abnormalities similar to those described in Caucasian patients, and that the aetiology of obstructive sleep apnoea in obese patients may be different from that in non-obese patients. In obese patients, upper airway soft tissue enlargement may play a more important role in the development of obstructive sleep apnoea, whereas in non-obese patients, bony structure discrepancies may be the dominant contributing factors for obstructive sleep apnoea.

Adult↗
PubMed2006

Obesity and hypertension in an Iranian cohort study; Iranian women experience higher rates of obesity and hypertension than American women.

BACKGROUND: Once considered as the main public health problem in developed countries, obesity has become a major problem throughout the world and developing countries, like Iran, are joining the global obesity pandemic. We determined the prevalence of overweight, obesity, and hypertension in a large cohort of Iranians and compared age-adjusted rates with the rates in the US. METHODS: Golestan Cohort Study is a population-based study of 8,998 men and women, aged 35-81 years, from urban and rural areas. Anthropometric parameters were measured by interviewers. Prevalence rates were directly adjusted to the 2000 United States standard population. RESULTS: The age-adjusted prevalence rates of overweight (BMI > or = 25 kg/m2) and obesity (BMI > or = 30 kg/m2) in this Iranian population were 62.2% and 28.0%, respectively. Both overweight and obesity were more common in women than men. Age-adjusted prevalence of overweight was significantly higher in Iranian women compared to the American women (68.6% vs. 61.6%), while the age-adjusted prevalence of obesity is closer in these two populations (34.9% vs. 33.2%). Iranian men-compared to American men-had significantly lower age-adjusted prevalence of overweight (53.7% vs. 68.8%) and obesity (16.2% vs. 27.5%). Age-adjusted prevalence of hypertension was higher in Iranian women than American women (35.7% vs. 30.5%). Diabetes mellitus was reported in 6.2% of participants. Mean waist-to-hip ratio (WHR) among women was 0.96. Smoking rates in men and women were 33.2% and 2.2%, respectively. CONCLUSION: The prevalence of obesity, overweight, and hypertension in Iran is as high as the US. However, Iranian women are more obese than American women and Iranian men are less obese than their American counterparts. This discrepancy might be due to the low rate of smoking among Iranian women. Iranian women have higher mean WHR than what WHO has defined in 19 other populations.

Adult↗
PubMed1983

Pancreatic polypeptide responses to protein meal challenges in obese but otherwise normal children and obese children with Prader-Willi syndrome.

Children with hyperphagia and obesity of Prader-Willi syndrome (PWS) have previously been shown to have blunted pancreatic polypeptide (PP) response to low protein meal stimulation. To evaluate the effects of various protein challenges on PP release in children with PWS, we administered both a low protein (0.2 g/kg) and a high protein (2.0 g/kg) meal stimulation test to 12 children previously diagnosed as having PWS and to an age- and weight-matched group of 19 obese but otherwise normal children. Serum samples were collected just before and for 3 h after meal ingestion. The mean (+/- SD) age was 11.7 +/- 4.2 yr for the PWS group and 10.3 +/- 3.8 yr for the obese group (P = 0.323). The percent ideal body weight for height for the PWS group (mean +/- SD 186 +/- 48%) was not significantly different from the percent ideal body weight for height for the obese group (174 +/- 35%; P = 0.421). Peak PP responses were significantly less for the PWS group than for the obese group for both the low and high protein meal stimulations. The mean (+/- SE) peak PP response with the low protein meal was 76.1 +/- 13 pg/ml for the PWS group and 302 +/- 93 pg/ml for the obese group (P less than 0.05). The mean peak response with the high protein meal was 181 +/- 51 pg/ml for the PWS group and 581 +/- 127 pg/ml for the obese group (P less than 0.01). Glucose rises were similar for both tests, although the PWS group did have a slightly smaller rise in glucose after the low protein stimulation than was observed in the obese group. The insulin response was also significantly less for the low protein meal in the PWS group compared to the low protein insulin response of the obese group. There were no significant differences in the insulin responses observed in both groups with the high protein meal test. This study confirms our previous observation and suggests that many children with PWS have a functional deficiency of PP. Our current study demonstrates that this condition is not a result of their obese condition or an alteration in their response threshold to protein.

Adolescent↗
PubMed2002

A genetic "obesity risk index" for patients with morbid obesity.

BACKGROUND: The influence of genetics on obesity is well established. Adoption studies and twin studies suggest that about 80% of the obesity risk is genetic. We designed a tool to predict outcomes of treatments in patients with sporadic or familial obesity. METHODS: Two factors best correlate with multifactorial genetic risk: 1) familial history and 2) age of onset. 147 morbidly obese adults self- or physician-referred for possible surgery for morbid obesity (age 17-66 y, BMI 35-82) were studied. Six elements were selected to measure the genetic influence on patients' weight: 3 personal weight milestones (weight at age 10, 20 and 30), and 3 family history factors (parents' weight, siblings' weight and second degree relatives' weight. These 6 elements of personal and family history information were collected prospectively on 35 obese patients and a feasible scoring system devised, with 0 points signifying no genetic component and 100 points suggesting the maximal possible genetic risk for obesity. Prospective data were then collected on 147 consecutive patients seen in consultation for possible bariatric surgery, to provide this "obesity risk index" (ORI). RESULTS: The final scoring system for the ORI assigned 50 possible points for personal weight milestones and 50 possible points for family history factors. At age 10, patients receive 10 or 20 points for being 2 or 3 SD above the mean BMI for age, respectively. At age 20, 10 or 20 points are received for BMI > 30 or 40, respectively. At age 30, 5 or 10 points are received for BMI > 35 or 50, respectively. 0 to 28 points are awarded for parental obesity, with 7 or 14 points for each parent with BMI > 30 or 40, respectively. The mean BMI of all siblings was calculated, with 6 or 12 points received for mean BMI greater than 30 or 40, respectively. Two points are awarded for each second degree relative with BMI > 35, to a maximum of 10 points. The mean (+/- SEM) score for our first 114 patients was 32 +/- 2 (range 0 to 87). The median score was 28.13% of patients had scores < 10; conversely, 13% scored points on all 6 elements. CONCLUSION: An ORI has been devised to quantify the genetic contribution to an individual's weight. Using this scoring system, we found that about 85% of patients who are candidates for bariatric surgery have elements in their history to suggest a genetic risk for morbid obesity. About 15% have extremely strong genetic ORIs.

Age of Onset↗
PubMed1991

A comparison of measurements of lean body mass derived by bioelectrical impedance, skinfold thickness and total body potassium. A study in obese and non-obese normal subjects.

The measurement of body composition is an important part of metabolic and epidemiological research, but most currently available methods are complex and expensive. We have, therefore, compared measurements of fat mass (FM) and lean body mass (LBM), obtained using a commercially available bioelectrical impedance monitor (The Holtain Body Composition Monitor) (IMP), and by measuring skinfold thickness (SFT), with values obtained by measuring total body potassium (TBK). Twenty subjects, 10 with a body mass index (BMI) less than 30 (kg m-2), (non-obese) and 10 with BMI greater than or equal to 30 (obese) took part in the study. There was a strongly significant linear relationship between LBM calculated from TBK and that calculated from impedance (IMP), in both non-obese and obese groups analysed separately (non-obese: r = 0.92; p less than 0.001 and obese: r = 0.92; p less than 0.001) and together (all: r = 0.89; p less than 0.001). LBM calculated from TBK was strongly linearly correlated with values derived from SFT for non-obese (r = 0.91; p less than 0.001) but not for obese subjects. Mean values of LBM of non-obese subjects derived by each method were not significantly different (TBK: 51.3 +/- 10.40 kg; IMP: 53.18 +/- 10.37 kg; SFT: 48.87 +/- 9.48 kg), but significant differences existed when the subjects were obese (TBK: 51.86 +/- 9.65 kg; IMP: 58.69 +/- 8.55 kg; SFT: 67.61 +/- 8.14 kg; p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Anthropometry↗
PubMed2001

[Changes and relations of leptin, growth hormone and insulin during puberty in obese and non-obese children].

In order to study the regularity of changing leptin, growth hormone (GH) and insulin (INS) during puberty and their relationships, a group of 300 obese and 300 non-obese children, aged 10-15 were selected. Leptin level increased with age and then decreased in boys, but it had only increasing tendency in girls. The GH level increased and then decreased suddenly in all groups. There was no obvious regularity in the change of INS. Serum leptin and INS levels were higher (P < 0.01) in obese children than that in non-obese children, while GH levels were significantly lower (P < 0.01) in obese boys. Results also showed that GH was negatively correlated with leptin in boys (obese group: r = -0.74, P < 0.05; non-obese group: r = -0.69, P < 0.05) and positively correlated with leptin in girls (obese group: r = 0.58, P < 0.05; non-obese group: r = 0.67, P < 0.01). There was a positive correlation between INS and leptin in non-obese girls (r = 0.54, P < 0.05). It is concluded that leptin might play an important role during the initial stage of puberty in children and the effect of leptin on pubescent development in girls is greater compared with boys. The correlation between leptin and GH are gender dependent in boys and girls, which may cause the timing differences of sudden growth in boys and girls.

Adolescent↗
PubMed2003

[From obesity to obesities: from concepts to practices].

In the singular, obesity is a symptom reflecting an excess of energy stores as fat mass, the only trait obese people are sharing. Long time ago we proposed to use the plural to account for the large diversity characterizing obese subjects that conceptual evolutions have put to the fore during the past three decades. Weight gain and obesity are resulting from a positive energy balance produced by the conjunction of a number of etiopathogenetic factors associated in various proportions according to patients and evolutive status. Decreasing physical activity, increasing sedentarity, quantitative and qualitative energy consumption unadapted to energy expenditure and to lipid oxidation capabilities, reinforced by psychological needs, are catching out the control of food intake, particularly since it is more efficient to defend against famine than to protect against plethora. These environmental factors, responsible for obesity pandemia, lead to obesity subjects predisposed by their genetic background, in itself extremely variable. The clinical heterogeneity of obesity is patent and a careful phenotypic analysis is a prerequisite to design the management strategy. Obesity is a chronic situation that needs a long-term treatment. The goals of treatment cannot be longer reduced to weight loss only, which in addition should be realistic, i.e. moderate. Management strategies must be conceived on a long-term basis, focused on prevention of weight regain, multifaceted and individually tailored. A number of tools are available and the state of the art is to use them appropriately to avoid being counter productive. Obesity may be viewed as an adaptive symptom in subjects poorly prepared to cope with recent environmental changes, but it is also a disease due to its prevalence, the number of weight dependent comorbidities and its socio economic costs. A specific medical approach of obesity has still to be developed.

Behavior Therapy↗
PubMed2006

Obesity prevention in pediatrics: A pilot pediatric resident curriculum intervention on nutrition and obesity education and counseling.

INTRODUCTION: Obesity is a highly burdensome public health issue associated with premature death, multiple comorbid disabilities and staggering healthcare costs. Between 1980-2000, the prevalence of obesity among children and adolescents nearly tripled. Obesity subjects youth to social stigmatization and discrimination. These economic and personal burdens mandate targeted prevention and detection educational programs for all individuals at risk. The most cost-effective method of approaching this obesity epidemic is through education of health professionals. METHODS: As part of an "Obesity Prevention in Pediatrics" curriculum, postgraduate-year (PGY)-2 residents first observed and then participated in the dietary evaluation and counseling of pediatric patients and their families. Attitudinal questionnaires, multiple-choice knowledge examinations and a pre-established checklist of desired skills and behaviors provided evaluation of the curriculum's effect on the participants' ability and willingness to manage actually obese or at-risk pediatric patients and their families. RESULTS: Attitudinal survey and knowledge test scores from control PGY-3 residents generally confirmed that their knowledge and counseling skills on obesity prevention and management were well below expectation. Following participation in the curriculum, study residents' knowledge tended to improve, as did their level of comfort in counseling obese and at-risk children, adolescents and their parents. CONCLUSION: Implementation of an "Obesity Prevention in Pediatrics" curriculum appears to improve participants' knowledge base as well as their skills and level of personal comfort in the recognition, evaluation and management, including counseling, of both obese and at-risk pediatric patients and their families.

Counseling↗
PubMed1991

[Significance of gender of obese children and body weight of parents and siblings for the results of the treatment of obesity in childhood].

We studied the influence of family size, family history of obesity, and the obese children's sex on the short and medium term outcome of an obesity therapy in children aged 10.7 +/- 3 years with mean percentage overweight of 41.4 +/- 16.9%. Family parameters such as obesity on other family members, single child families, and sex of the obese children did not influence the decision to stop or to complete therapy. Boys were more successful in weight reduction than girls both after 3-6 months and after 3-5 years; the difference being not significant, however. Children without family history initially were significantly less overweight than those with familial obesity, and they exhibited the best short and medium term results. Children of obese families initially were the fattest ones. They reduced their weight more than average, but they tended to regain weight during the following 3-5 years, reaching the highest levels of overweight after that time. Children without family history of obesity did not regain weight, however. Thus even after good short term results obese children of obese parents should be regarded at risk for relapse and should be checked for years after therapy to prevent weight regain.

Body Weight↗
PubMed1994

[Insulin resistance in obese and non-obese patients with polycystic ovary syndrome. Possible role in the pathogenesis of the disease].

The pathogenesis of Polycystic Ovary Syndrome (PCOs) is not well known till now. Previous reports indicated an hyperinsulinemia and insulin resistance in obese and non obese PCOs. However the role of hyperinsulinemia in PCOs pathogenesis is not completely understood. In this study we evaluated the glycemic and insulinemic response to OGTT in 21 women suffering from PCOs (13 obese and 8 normal weight) and in 16 fertile women as a control group (8 obese and 8 normal weight). All tested women showed normal glycemia before and after OGTT. Basal insulinemia in PCOs was similar to that observed in control group. Mean insulinemic levels following OGTT in obese control group and in PCOs were significantly higher than those observed in normal women (p < 0.05). Insulin area under curve (AUC) following OGTT in non obese PCOs was significantly higher than that observed in non obese control women (72442.13 +/- 18668.9 mUI/ml/h versus 53710.8 +/- 83365 mUI/ml/h; p = 0.02), but lower than that observed in obese PCOs (192793 +/- 49421; p < 0.001). In obese PCOs insulin AUC was significantly higher than that observed in obese control group (138836.8 +/- 28800.9; p = 0.012). Insulin AUC was positively related to BMI in control group (p < 0.001) but not in PCOs. In PCOs group insulin AUC was positively related to hirsutism degree (p = 0.032) and circulatory levels of T (p = 0.044), LH (p < 0.001) and E1 (p = 0.026).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1993

Validity and reproducibility of a self-administered dietary questionnaire in obese and non-obese subjects.

The validity and reproducibility of a self-administered dietary questionnaire has been tested with specific attention to differences between obese and non-obese subjects. To test the validity, the dietary questionnaire was compared with 4-day food records, 24-h energy expenditure (24EE) and nitrogen excretion in 45 obese and 19 non-obese men and women. Energy intake was 2% higher (non-significantly) from questionnaire than from food records in the non-obese, but 35% higher (P < 0.001) in the obese. Comparing energy intake from the questionnaire with estimated 24EE, the questionnaire gave 4% higher values in both the non-obese and obese, differences which were not significant. The reproducibility in the obese sample that completed the questionnaire twice was comparable to that observed in normal populations. These data suggest that it is possible to obtain information on obese subjects' dietary intake that is at least as valid and reproducible as that from normal weight individuals.

Adult↗
PubMed1987

Plasma fluoride concentration and urinary fluoride excretion in obese and non-obese patients following enflurane anesthesia.

Plasma fluoride concentrations and urinary fluoride excretions were measured following enflurane anesthesia (1.5%, 2 hours) in obese (8 cases) and non-obese (9 cases) patients. At the end of anesthesia, there was no significant difference in plasma fluoride concentrations between the two groups. In the several days following anesthesia, however, plasma fluoride concentrations in obese patients were higher than those in non-obese patients. Urinary fluoride excretions after anesthesia were greater in obese patients than those in non-obese patients, and the period of increased fluoride excretion was prolonged in obese patients. These results suggested that obese patients metabolized more enflurane than non-obese patients during the postanesthetic period. In obese patients, their excess fatty tissue may cause a greater and more prolonged elevation of blood enflurane concentrations after anesthesia.

Journal Article↗
PubMed2004

The obesity syndrome and acanthosis nigricans. Acanthosis nigricans is a common cosmetic problem providing epidemiological clues to the obesity syndrome, the insulin-resistance syndrome, the thrifty metabolism, dyslipidaemia, hypertension and diabetes mellitus type II.

Obesity and its consequences are arguably the chief public health problems facing the developed world. Obesity causes many fatal diseases, in particular cerebrovascular and cardiovascular disease. Acanthosis nigricans (AN) is a common cosmetic disability in pigmented ethnic groups. It may present with periorbital darkening or darkening of the neck or knuckles as well as acrochordons (skin tags) around eyelids, neck or axillae. The more classical AN of axillae and groins is less often a cosmetic disability, although it is an important physical sign. AN is very common in pigmented populations throughout the world, irrespective of domicile. It is rare in whites. AN is closely associated with all the features of the insulin-resistance syndrome (IRS), especially obesity. AN and IRS share a similar prevalence and epidemiology. IRS (also known as syndrome X or the deadly quartet) is characterized by insulin resistance (IR) and its associated conditions, including obesity, dyslipidaemia, hypertension and diabetes mellitus (DM) type II. The sequelae of IRS are cardiovascular and cerebrovascular disease. The origins of insulin resistance and its sequel, IRS, are debated. Insulin resistance can result from obesity. Also obesity usually presents before AN, hypertension or DM II. For these reasons it may be more helpful to recognize instead an obesity syndrome. The obesity syndrome is characterized by a genetically determined thrifty metabolism that protects subjects in famine conditions but which, in conditions of plenty, leads to weight gain with all its consequences, including hyperlipidaemia, hypertension, IR with DM II, and, in due course, cerebrovascular and cardiovascular disease. In pigmented races, AN is an important early manifestation of the obesity syndrome. AN helps identify persons at particular risk of developing the obesity syndrome, dyslipidaemia, hypertension and IR with DM II. Recognition of AN, therefore, offers important opportunities for health screening and preventative medicine.

Journal Article↗
PubMed1995

Cloning of rat obese cDNA and its expression in obese rats.

The mouse obese gene product, expressed specifically in adipose tissue, regulates energy balance in mice. Mutation of the obese gene results in marked obesity and type II diabetes as part of a syndrome that resembles morbid obesity in humans. Here we report the cloning and sequencing of rat obese cDNA. Neither alterations of nucleotide sequence in the coding region nor changes of the gene structure were found in two rat strains with obesity, Zucker (fa/fa) and Otsuka Long Evans Tokushima Fatty. The expression level of obese mRNA in adipose tissue of Zucker (fa/fa) rat was found to be about 4 times that in lean littermates, suggesting some mutation or abnormal expression of the receptor for the obese product in obese rats of this strain.

Animals↗