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Biomedical subjects

E Ravussin

Publications and source records attributed to E Ravussin.

At least 127 records · Page 7Linked to original sources
PubMed1995

Intracellular magnesium and insulin resistance: results in Pima Indians and Caucasians.

Intracellular magnesium is a cofactor for numerous enzymes involved in carbohydrate metabolism. Magnesium accumulation is dependent upon insulin action and correlates with insulin-mediated glucose uptake. As Pima Indians are known to be insulin resistant, we investigated whether, in response to insulin infusion, they have lower erythrocyte magnesium accumulation than Caucasians. Insulin-mediated glucose uptake was determined by a euglycemic hyperinsulinemic glucose clamp in 29 obese nondiabetic volunteers: 15 Caucasians (8 males and 7 females) and 14 Pima Indians (8 males and 6 females). Pima Indians were younger than Caucasians (mean +/- SD, 28 +/- 7 vs. 39 +/- 8 yr; P < 0.01), but had similar body mass index and fasting/2-h plasma glucose concentrations. Despite higher steady state plasma insulin levels (692 +/- 260 vs. 540 +/- 70 pmol/L; P < 0.03), Pima Indians had lower insulin-mediated glucose uptake than Caucasians (108 +/- 20 vs. 244 +/- 32 mg/m2.min; P < 0.0001). The mean fasting plasma magnesium concentration was lower in Pima Indians than in Caucasians (0.79 +/- 0.05 vs. 0.85 +/- 0.06 mmol/L; P < 0.01), whereas the mean fasting erythrocyte magnesium concentrations (1.98 +/- 0.10 vs. 2.03 +/- 0.14 mmol/L) were similar in the 2 groups. In response to insulin infusion, erythrocyte magnesium content increased less in Pima Indians than in Caucasians (0.15 +/- 0.07 vs. 0.28 +/- 0.21 mmol/L; P < 0.03). However, this increase was similar in the 2 groups when values were adjusted for insulin-mediated glucose uptake. In conclusion, nondiabetic Pima Indians have a lower erythrocyte magnesium accumulation in response to insulin infusion; this is probably due to their high degree of insulin resistance. The biochemical and physiological consequences of decreased intracellular magnesium uptake are discussed.

Adult↗
PubMed1995

Reduced insulin secretion: an independent predictor of body weight gain.

A causal role in the pathogenesis of obesity has been proposed for hyperinsulinemia and insulin resistance in populations with a high prevalence of a "thrifty genotype." An alternative hypothesis is that obesity-induced hyperinsulinemia is an adaptation which, by increasing central nervous system insulin signaling (which suppresses food intake), confers resistance to weight gain. To characterize the relationship between the level of insulin secretion and the risk of weight gain, we examined whether any of three different measures of the level of insulin secretion (the area under the plasma insulin curve during both a meal tolerance test and an oral glucose tolerance test, and the acute insulin secretory response to iv glucose) was predictive of weight gain in a prospective study of 97 Pima Indians (64 males and 33 females) with normal glucose tolerance. During a mean (+/- SD) follow-up period of more than 3 yr (males, 3.58 +/- 1.46 yr; females, 3.02 +/- 1.73 yr), average weight increased 2.1 +/- 3.0%/yr in males and 3.5 +/- 3.6%/yr in females, reflecting a mean annual increase in body fat content of 6.9%/yr in both sexes. Insulin secretion was negatively associated with the rate of weight gain, whether assessed by the insulin response during the meal tolerance test (r = -0.35; P < 0.001), the oral glucose tolerance test (r = -0.30; P = 0.004), or the acute insulin secretory response to iv glucose (r = -0.28; P = 0.002). Moreover, the significance of the relationship between each measure of insulin secretion and weight gain persisted after controlling for differences in age, sex, initial body weight, and insulin sensitivity. Relatively reduced insulin secretion, therefore, is a significant and independent predictor of the tendency to gain weight and adiposity in Pima Indians. The presence of relative insulin resistance also conferred an independent reduction in the risk of weight gain in some regression analyses. We conclude that insulin resistance and hyperinsulinemia are unlikely to play a causal role in the development of obesity, and that relatively reduced insulin secretion is a marker of an increased risk of weight gain in this population. These conclusions support the hypothesis that the level of insulin secretion plays an important role in long term body weight regulation.

Adipose Tissue↗
PubMed1995

Spontaneous overfeeding with a 'cafeteria diet' in men: effects on 24-hour energy expenditure and substrate oxidation.

OBJECTIVE: To investigate the relationship between obesity and ad libitum food intake (quantity and composition) and to assess the impact of ad libitum food intake on energy expenditure and macronutrient oxidation. DESIGN: Male volunteers were first fed a weight maintaining diet for at least 4 days before selecting their food for the next 5 days from two computerized vending machines offering a variety of familiar, palatable foods. 24-h energy expenditure (24EE) and substrate oxidation were measured in a respiratory chamber on the last day of each weight maintenance and ad libitum intake periods. SETTING: Ten day admission on a metabolic research ward. SUBJECTS: Thirty-four non-diabetic Pima Indian males covering a wide range of body weight and body composition (30 +/- 8 y, 102.1 +/- 30.2 kg, 34 +/- 9% body fat, mean +/- s.d.). RESULTS: Weight maintenance requirements averaged 2913 +/- 342 kcal/d. Energy intake during the ad libitum period increased to 4550 +/- 921 kcal/d (12 +/- 1% protein, 40 +/- 4% fat, 48 +/- 4% carbohydrate) i.e., a spontaneous overeating by 54 +/- 32% above weight maintenance requirement, resulting in a 0.9 +/- 1.0 kg body weight gain. Neither the composition of the selected diet nor the degree of overeating was associated with physical characteristics, such as body weight and body composition. When compared with baseline, spontaneous overeating on day 5 was associated with a 396 +/- 233 kcal/d increase in 24EE, a 607 +/- 503 kcal/d increase in carbohydrate oxidation, a 214 +/- 392 kcal/d decreased in lipid oxidation (P < 0.01), and no change in protein oxidation. Increased carbohydrate oxidation correlated with the excess carbohydrate intake (r = 0.69, P = 0.0001) accounting for 68 +/- 13% (mean +/- s.e.e.) of the excess, whereas excess fat intake was not oxidized. CONCLUSION: In response to spontaneous overfeeding on a mixed 'cafeteria diet', excess carbohydrate intake is oxidized, suggesting a physiological control of carbohydrate stores, whereas excess fat intake is channeled toward fat stores. None of the observed changes were related to indices of obesity.

Adult↗
PubMed1995

Racial difference in body core temperature between Pima Indian and Caucasian men.

A low body temperature is associated with a low metabolic rate for a given body size and body composition. These two traits might have been assets in the history of a population subjected to cycles of feast and famine, but became part of an obesity-prone syndrome in our westernized society characterized by plenty of food and a sedentary lifestyle. We tested whether Pima Indians have lower body temperatures than Caucasians, a trait which might partly explain the high prevalence of obesity in this population. Twenty-five Pima Indian (28 +/- 6 yrs, 87.8 +/- 22.8 kg, 29 +/- 9% body fat) and 25 Caucasian (30 +/- 5 yrs, 80.7 +/- 18.4 kg, 22 +/- 11% body fat) men had body core temperatures measured by telemetry for 24 h while in a respiratory chamber. Mean daily body core temperature was 36.93 +/- 0.12 and 36.90 +/- 0.22 degrees C in Pima Indians and Caucasians, respectively. Since body core temperature during sleep (SLBCT) correlated with percentage body fat, a subset of 10 Pima Indians and 10 Caucasians were pair-matched for body weight and percentage body fat. In this group, SLBCT was lower in Pima Indians than in Caucasians (36.45 +/- 0.10 vs 36.65 +/- 0.27 degrees C; P < 0.01) and, ethnic group accounted for 20% of the variance in SLBCT (P < 0.01). Surprisingly, the lower SLBCT was not associated with a low metabolic rate and therefore does not seem to play a role in the etiology of obesity in Pima Indians.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗
PubMed1995

Food intake and energy expenditure in obese female bingers and non-bingers.

Since compulsive eating occurs in approximately 30% of obese females and is associated with earlier relapse following weight loss, we compared daily energy intake, dietary composition and energy expenditure among obese binge eaters and obese non-bingers. Nine obese bingers (33 +/- 4 yrs, 95 +/- 6 kg, 39 +/- 1% fat) and nine obese non-bingers (47 +/- 3 yrs, 93 +/- 5 kg, 40 +/- 1% fat) were admitted for 12 days to a metabolic unit. Binge eaters were defined as scoring > 25 on the binge eating scale (BES). During the initial 8 days, subjects ate ad libitum from two computerized vending machines offering a variety of foods and beverages. A weight maintenance diet was then provided for the next 4 days. Twenty-four hour energy expenditure (24EE) and respiratory quotient (24Q) were measured on the last day of both feeding periods in a respiratory chamber. Obese bingers showed a wider range of energy intake compared to non-bingers, but the mean daily energy intake was similar between the two groups (2587 +/- 454 vs 2386 +/- 201 kcal/d) during 8 days of ad libitum intake. 24EE was not different between bingers and non-bingers after 8 days of ad libitum intake (2298 +/- 147 vs 2109 +/- 97 kcal/d, P = 0.3) or 4 days of weight maintenance diet, even more so after adjustment for differences in fat-free mass, fat mass and age. Resting metabolic rate, sleeping metabolic rate, and macronutrient intake and oxidation were also similar between groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1995

Daily energy expenditure in male endurance athletes with differing energy intakes.

The 24-h energy expenditure (24-h EE), resting EE (REE), sleeping EE (SEE), and spontaneous physical activity (SPA) were compared between six male endurance athletes whose reported energy intake was low (LOW) and did not match that theoretically required for weight maintenance and four whose reported energy intake appeared adequate (ADQ) and matched their estimated EE. Groups did not differ in age, body weight, fat-free mass, and daily EE estimated from activity records. The LOW athletes reported an energy intake 6338 +/- 2164 kJ.d-1 less than estimated EE. The 24-h EE, REE, SEE, and SPA of the LOW athletes were significantly lower than the ADQ athletes (862, 523, 770 kJ.d-1, and 43 min.d-1, respectively). Using all subjects, there was a significant positive correlation between REE and free thyroxine (FT4) (r = 0.82) and SEE and FT4 (r = 0.66). Thus, part of the LOW athlete's ability to maintain body weight on a seemingly low energy intake appears due to a lower daily sedentary EE.

Activities of Daily Living↗
PubMed1995

Low resting metabolic rate as a risk factor for weight gain: role of the sympathetic nervous system.

Resting metabolic rate (RMR) comprises 50-80% of daily energy expenditure, and is highly variable between subjects even after adjusting for body weight and body composition. RMR is believed to be genetically determined. Individuals with a low RMR for a given body size are at higher risk of significant weight gain, relative to those with a high RMR. Studies in Caucasians indicate that sympathetic nervous system (SNS) activity is related to the three major components of energy expenditure: RMR, the thermic effect of food and spontaneous physical activity. Pima Indians have low SNS activity and, unlike Caucasians, their RMR does not correlate with SNS activity. A variant of the beta 3-adrenoceptor gene has been found to be weakly associated with metabolic rate. Low resting SNS activity and its apparent dissociation from metabolic rate could be a causative factor in the development of obesity.

Body Composition↗
PubMed1994

Do obese eat faster than lean subjects? Food intake studies in Pima Indian men.

Food intake rate has previously been derived from observation of eating behavior in laboratory settings or in public eating establishments. Although it has been suggested that obese individuals eat faster than lean individuals, observations of such an "obese eating style" have yielded mixed results. In the present study, the relationship between ad-libitum food intake rate and obesity was evaluated over 4 days on a metabolic ward in 28 healthy Pima Indian men (Mean +/- SD; 29 +/- 7 y, 100.4 +/- 27.1 kg, 33 +/- 10% body fat) using an automated food selection system containing a large variety of foods. Total energy intake averaged 18829 +/- 3299 kJ/d consisting of 47 +/- 4, 40 +/- 3, and 13 +/- 1 percent of carbohydrate, fat and protein, respectively. The average meal duration was 25 +/- 7 min. Food intake rate was 68 +/- 21 g/min while carbohydrate, fat and protein intake rates were 23 +/- 6, 9 +/- 3 and 6 +/- 2 g/min, respectively. Food intake rate correlated negatively with % body fat (r = -0.61, P < 0.01). Similar relationships were found between the intake rates of carbohydrate, fat and protein and body fatness. Only prospective studies will indicate whether a slow food intake rate may contribute to the etiology of obesity by possibly reducing satiety.

Adult↗
PubMed1994

Energy intake and physical activity in Pima Indians: comparison with energy expenditure measured by doubly-labeled water.

To test the validity of survey techniques for measuring diet and activity patterns of Pima Indians, sequential 24-hour recalls, a food frequency questionnaire (FFQ), and an activity questionnaire were compared to free-living energy expenditure. Total energy expenditure (TEE) measured by doubly labeled water was 13.27 +/- 2.95 MJ/d for the 12 males (mean +/- SD: 35 +/- 14 yr; 97 +/- 35 kg; 32 +/- 9% body fat) and 11.67 +/- 1.85 MJ/d for the 9 females (31 +/- 13 yr; 106 +/- 32 kg; 49 +/- 6% body fat). Energy intake assessed by 24-hour recall was 13.59 +/- 7.81 MJ/d for men and 9.29 +/- 2.77 MJ/d for women, compared to 12.84 + 2.85 and 9.40 + 2.61 MJ/d for men and women, respectively, by FFQ. Both dietary methods indicated significant underreporting by women when compared to TEE. Energy intake assessed by FFQ was significantly correlated with TEE (r=0.48, p=0.03). This was true with 24-hour recall energy intake only when data from two extremely large alcohol consumers were eliminated (r=0.64, p=0.03, N=19). Although a low level of activity was apparent, the activity questionnaire produced significant correlations with measurements of energy expenditure and therefore represents an important tool for examining the relationship between physical activity and diseases.

Adult↗
PubMed1994

Whole-body energy metabolism and skeletal muscle biochemical characteristics.

A low metabolic rate for a given body size and a low fat versus carbohydrate oxidation ratio are known risk factors for body weight gain, but the underlying biological mechanisms are poorly understood. Twenty-four-hour energy expenditure (24EE), sleeping metabolic rate (SMR), 24-hour respiratory quotient (24RQ), and forearm oxygen uptake were compared with respect to the proportion of skeletal muscle fiber types and the enzyme activities of the vastus lateralis in 14 subjects (seven men and seven women aged 30 +/- 6 years [mean +/- SD], 79.1 +/- 17.3 kg, 22% +/- 7% body fat). The following enzymes were chosen to represent the major energy-generating pathways: lactate dehydrogenase (LDH) and phosphofructokinase (PFK) for glycolysis; citrate synthase (CS) and beta-hydroxyacl-coenzyme A dehydrogenase (beta-OAC) for oxidation; and creatine kinase (CK) and adenylokinase (AK) for high-energy phosphate metabolism. Forearm resting oxygen uptake adjusted for muscle size correlated positively with the proportion of fast-twitch muscle fibers (IIa: r = .55, P = .04; IIb: r = .51, P = .06) and inversely with the proportion of slow oxidative fibers (I: r = -.77, P = .001). 24EE and SMR adjusted for differences in fat-free mass, fat mass, sex, and age correlated with PFK activity (r = .56, P = .04 and r = .69, P = .007, respectively). 24RQ correlated negatively with beta-OAC activity (r = -.75, P = .002). Our findings suggest that differences in muscle biochemistry account for part of the interindividual variability in muscle oxygen uptake and whole-body energy metabolism, ie, metabolic rate and substrate oxidation.

Adult↗
PubMed1994

Energy and macronutrient metabolism.

In general, obesity is a state of high energy stores, high energy intake, and high energy expenditure. The high energy expenditure is largely due to the increased fat-free mass. The failure to find a positive relationship between reported energy intake and body size reflects a greater under-reporting of calorie intake among obese individuals. Obesity, therefore, develops as a consequence of a chronic imbalance between intake and expenditure, although the cause of this is not apparent from the energy balance equation. However, this equation can be dissected into its component nutrient balance equations because net de novo lipogenesis is negligible in free-living humans. Fat calories are handled very differently from non-fat calories. Non-fat nutrient oxidation rates rise and fall to match the fluctuations in non-fat intake so that non-fat calorie balance is actively maintained. In contrast, changes in fat intake do not acutely affect fat oxidation but are matched by changes in storage. Therefore, within the fat balance equation there is ample scope for a chronic imbalance between fat intake and oxidation. Also, there is some evidence that carbohydrate balance may be an important signal for hunger and satiety. These concepts imply that, under free-living, ad libitum eating conditions, changes in nutrient intake composition (e.g. an increased proportion of fat in the diet) or changes in nutrient oxidation composition (e.g. a decrease in the proportion of fat oxidized) will lead to body weight change (in these cases, to weight gain). Considering obesity as a consequence of normal physiology (with its normal variation between individuals) in a 'pathological' environment (high fat diet, low exercise) offers an important perspective for explaining the interpopulation and interindividual differences in obesity and for formulating treatment and prevention options. Low energy expenditure (relative to body size), high respiratory quotient and insulin sensitivity have been shown to be predictors of weight gain, although upon gaining weight these metabolic factors tend to 'normalize'. Metabolic responses to underfeeding or overfeeding are largely predictable from the changes in calorie intake and changes in body composition, but some adaptive changes may occur.

Body Weight↗
PubMed1994

Body fat distribution and energy metabolism in obese men and women.

OBJECTIVE: Upper body obesity seems to be associated with a better prognosis for weight loss than does lower body obesity. However, the impact of body fat distribution on energy metabolism is not clear. SUBJECTS: One hundred fifteen non-diabetic obese Caucasians (64 males and 51 females) and 108 Caucasian lean controls (82 males and 26 females) were studied. METHODS: Body composition was assessed by hydrodensitometry and body fat distribution was estimated by the waist-to-thigh circumference ratio (W/T). Values of 24-hour energy expenditure (24h-EE), basal metabolic rate (BMR), sleeping metabolic rate (SMR) and respiratory quotient (RQ) were measured in a respiration chamber. RESULTS: BMR, adjusted for differences in fat-free mass, fat mass, age and sex, correlated with W/T in obese males (r = 0.40; p < 0.01), but not in obese females. Obese male subjects with upper body obesity had BMR significantly higher than those with lower body obesity (2189 +/- 268 vs 1974 +/- 141 kcal/day; p < 0.01), independently of differences in fat-free mass, fat mass and age. No correlations were found between W/T and adjusted 24h-EE, SMR or RQ in all examined groups. CONCLUSION: These findings indicate that in obese males, upper body obesity is associated with increased metabolic rate, possibly related to higher levels of lipid turnover in visceral fat.

Adipose Tissue↗
PubMed1994

Determinants of total daily energy expenditure: variability in physical activity.

Excessive energy intake and/or reduced total daily energy expenditure (TEE) causes obesity. To determine the relationship between obesity and TEE in an obesity-prone population, we measured TEE, 24-h sedentary energy expenditure (SEDEE), and basal metabolic rate (BMR) in 30 Pima Indian men (83.6 +/- 20.0 kg and 31 +/- 9% fat) by the doubly labeled water method and a respiratory chamber. The energy expenditure for physical activity (EEACT) was calculated as TEE - (BMR + 0.1 TEE), where 10% of TEE is an estimate of the thermic effect of food. Fat-free mass was the best single determinant (P < 0.01) of TEE, explaining 48% of its variance. TEE, SEDEE, BMR, and EEACT were 12,010 +/- 2292, 9945 +/- 1559, 7677 +/- 1901, and 3297 +/- 1732 kJ/d, respectively. Because EEACT is dependent on body weight, EEACT/kg body wt (41.7 +/- 23.2 kJ.d-1.kg-1) and TEE/(BMR + 0.1 TEE) (1.39 +/- 0.22) were used as indexes of the level of physical activity. Both indexes correlated negatively with percent body fat (r = -0.56, P < 0.01 and r = -0.42, P < 0.03, respectively). These results suggest that obesity is associated with lower levels of physical activity.

Adult↗
PubMed1994

Relationship between sleep stages and metabolic rate in humans.

Differences in sleeping metabolic rate (SMR) among subjects may be related to different levels of energy expenditure associated with sleep stages. The relationship between energy expenditure and sleep stages was investigated overnight in 29 subjects (14 Caucasians and 15 Pima Indians, 18 males and 11 females; mean +/- SD, 31 +/- 7 yr, 83 +/- 26 kg, 27 +/- 11% fat). Sleep stages were determined by electroencephalogram recording, whereas energy expenditure was measured in a 1,000-liter Plexiglas sleep box constructed around a bed as a fast-response open-circuit indirect calorimeter. Eighty-five percent of the interindividual variability in SMR was explained by differences in fat-free mass, fat mass, age, sex, and race (r2 = 0.85). The intra-individual variance in SMR over time was related to sleep stages and to clock time. Within subjects, SMR in stage 3 was significantly lower than in stage 2 (-39 +/- 18 kcal/day; P < 0.05) and rapid eye movement sleep (-51 +/- 23 kcal/day; P < 0.05). Also, sleep stages were associated with different respiratory quotients. Because sleep stages are associated with only small differences in energy metabolism, our results suggest that sleep stages play a minor role in the variance of SMR among subjects. However, the duration of sleep may contribute to the variability of 24-h energy expenditure.

Adult↗
PubMed1994

Muscle sympathetic nerve activity in response to glucose ingestion. Impact of plasma insulin and body fat.

Carbohydrate intake stimulates sympathetic nervous system activity in lean subjects, whereas in obese subjects, the results have been inconsistent. The aim of this study was to directly measure sympathetic neural outflow to skeletal muscle in response to a 75-g oral glucose tolerance test (OGTT) in 15 Pima Indian and 16 Caucasian men, matched for body fat and age, but covering a large range of body weight (57-113 kg) and body fat (4-41%). Fasting muscle sympathetic nerve activity (MSNA) correlated positively with body fat (r = 0.73; P = 0.001) in Caucasians but not in Pima Indians, whereas the increase in MSNA during the OGTT correlated negatively with the percentage of body fat (r = -0.38, P = 0.03) independently of race. In each subject, the increase in MSNA over time correlated positively with the increase in plasma insulin levels, but the slopes of these relationships were inversely related to the percentage of body fat (r = -0.52, P = 0.003) independently of race. In conclusion, obesity is associated with a higher fasting sympathetic neural outflow to muscle but a blunted increase in response to an oral glucose load despite a larger increase in plasma insulin levels. This blunted response may represent another feature of the obesity/insulin resistance syndrome.

Adipose Tissue↗
PubMed1994

Effects of a traditional lifestyle on obesity in Pima Indians.

OBJECTIVE: The Pima Indians of Arizona have the highest reported prevalences of obesity and non-insulin-dependent diabetes mellitus (NIDDM). In parallel with abrupt changes in lifestyle, these prevalences in Arizona Pimas have increased to epidemic proportions during the past decades. To assess the possible impact of the environment on the prevalences of obesity and NIDDM, data were collected on members of a population of Pima ancestry (separation 700-1,000 years ago) living in a remote mountainous location in northwestern Mexico, with a lifestyle contrasting markedly with that in Arizona. RESEARCH DESIGN AND METHODS: Pima heritage was established by history and by use of Pima language. Measurements of weight, height, body fat (bioimpedance), blood pressure, plasma levels of glucose, cholesterol, and HbA1c were obtained in 19 women (36 +/- 13 years of age) and 16 men (48 +/- 14 years of age) and compared with sex-, age- and diabetes status-matched Pimas living in Arizona (10 Arizona Pimas for each Mexican Pima). RESULTS: Mexican Pimas were lighter (64.2 +/- 13.9 vs. 90.2 +/- 21.1 kg, P < 0.0001; means +/- SD) and shorter (160 +/- 8 vs. 164 +/- 8 cm, P < 0.01) with lower body mass indexes (24.9 +/- 4.0 vs. 33.4 +/- 7.5 kg/m2, P < 0.0001) and lower plasma total cholesterol levels (146 +/- 30 vs. 174 +/- 31 mg/dl, P < 0.0001) than Arizona Pimas. Only two women (11%) and one man (6%) had NIDDM, contrasting with the expected prevalences of 37 and 54% in female and male Arizona Pimas, respectively. CONCLUSIONS: This preliminary investigation shows that obesity, and perhaps NIDDM, is less prevalent among people of Pima heritage living a "traditional" lifestyle than among Pimas living in an "affluent" environment. These findings suggest that, despite a similar potential genetic predisposition to these conditions, a traditional lifestyle, characterized by a diet including less animal fat and more complex carbohydrates and by greater energy expenditure in physical labor, may protect against the development of cardiovascular disease risk factors, obesity, and NIDDM.

Adolescent↗
PubMed1994

Concentrations of adipsin in blood and rates of adipsin secretion by adipose tissue in humans with normal, elevated and diminished adipose tissue mass.

Adipsin, which is identical to complement factor D, is synthesized by fat cells, circulates in the bloodstream and is profoundly deficient in mice with genetic and hypothalamic obesity. With the recent cloning of human adipsin, a quantitative human immunoassay has been developed. In the present study, we measured adipsin blood concentrations in humans with increased and decreased adipose stores as well as adipsin secretion by adipose tissue obtained from lean and obese individuals. The results demonstrate that adipsin is released by human adipose tissue fragments as has previously been shown in mice, and that, in contrast to obese mice, blood adipsin concentrations were not reduced in the obese humans tested in this study. We also observed that blood adipsin concentrations can vary as a function of feeding or adiposity, in that they tend to be mildly elevated in obese individuals or mildly reduced in individuals with total lipo-atrophy, cachexia related to AIDS and anorexia nervosa. Thus, the circulating concentration of adipsin tends to correlate positively with degree of adiposity. Clearly, no deficiency in blood adipsin concentrations or adipsin secretion by adipose tissue was observed in the obese individuals studied.

Adipose Tissue↗