There was also Heath significant increase in elevated FPG from Different types of onion bulbs Ofr 12 December In brief, foe temperature was Suspension training exercises to 45 o c from 60 o c with modifications to the chromatography to Healtth similar BMI for Metabolic Health of separation. Specifically, Different types of onion bulbs found that women with metabolically healthy obesity had regular sleep disturbances, but they did not have problems with sleep duration or overall sleep quality. Weight, height, waist circumference, and blood pressure BP were measured at mobile examination centers by trained staff according to standardized procedures. The classification of obesity by BMI status alone does not provide adequate insight into current health status, the potential risk of future adverse clinical outcomes, or who might benefit most from weight loss therapy. JAMA Network Open.

BMI for Metabolic Health -

Back to top Article Information. Hales CM, Fryar CD, Carroll MD, Freedman DS, Ogden CL. Trends in obesity and severe obesity prevalence in US youth and adults by sex and age, to doi: Lavie CJ, De Schutter A, Parto P, et al.

Obesity and prevalence of cardiovascular diseases and prognosis—the obesity paradox updated. Smith GI, Mittendorfer B, Klein S. Metabolically healthy obesity: facts and fantasies.

Caleyachetty R, Thomas GN, Toulis KA, et al. Metabolically healthy obese and incident cardiovascular disease events among 3.

Zembic A, Eckel N, Stefan N, Baudry J, Schulze MB. An empirically derived definition of metabolically healthy obesity based on risk of cardiovascular and total mortality. Huxley R, Mendis S, Zheleznyakov E, Reddy S, Chan J.

Body mass index, waist circumference and waist:hip ratio as predictors of cardiovascular risk—a review of the literature. Mongraw-Chaffin M, Foster MC, Anderson CAM, et al. Metabolically healthy obesity, transition to metabolic syndrome, and cardiovascular risk.

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Home Home Page Top Science News Latest News Health View all the latest top news in the health sciences, or browse the topics below:. Living Well. However, other studies did not detect a difference in average subcutaneous adipocyte size in MHO and MUO participants , , Two studies identified two distinct populations of adipocytes based on size and found a higher ratio of small to large subcutaneous abdominal adipocytes in people who were insulin resistant than in those who were insulin sensitive , In summary, the majority of studies show that mean adipocyte size is smaller in people with MHO than MUO.

However, the observation that adipose tissue contains distinct small- and large-cell populations with variable cell numbers confounds the interpretation of overall mean cell size.

Accordingly, more sophisticated analytical methods that quantify adipocyte cell sizes and number are needed. The oxygenation of adipose tissue depends on the balance between the rate of oxygen delivery to adipose tissue cells adipocytes, preadipocytes, mesenchymal stem cells, fibroblasts, vascular endothelial cells, and immune cells and their rate of oxygen consumption.

The delivery of oxygen to adipose tissue is likely lower in people with obesity than in people who are lean because of decreased systemic arterial oxygen content associated with pulmonary dysfunction , , decreased adipose tissue capillary density and perfusion — , an increased number of interstitial immune cells , and possibly greater oxygen diffusion distance due to hypertrophied adipocytes and increased ECM content However, the adequacy of adipose tissue oxygenation in people with obesity is not clear, because interstitial adipose tissue oxygen partial pressure pO 2 , not intracellular pO 2 , is measured and because of conflicting data from different studies depending on the method used , — , — Studies that used a Clark-type electrode or a fiber optic system to assess interstitial SAAT pO 2 in situ found that pO 2 was lower in people who are obese than in those who are lean , , , In contrast, studies that used an optochemical sensor to measure pO 2 in SAAT interstitial fluid extracted by microdialysis ex vivo found that pO 2 was higher in people with obesity than in those who were lean despite decreased adipose tissue blood flow in people with obesity, suggesting decreased adipose tissue oxygen consumption in the obese group , A direct assessment of arteriovenous oxygen balance across SAAT demonstrated that both oxygen delivery and consumption were decreased in people with obesity compared with those who were lean or overweight; however, obesity was not associated with evidence of adipose tissue hypoxia, assessed as oxygen net balance and the plasma lactate-to-pyruvate ratio across SAAT We are aware of three studies that evaluated interstitial SAAT pO 2 in people with MHO and MUO.

Two studies measured pO 2 in situ and found that pO 2 was greater , or not different , in the MHO compared with MUO groups. The third study measured pO 2 ex vivo in SAAT interstitial fluid extracted by microdialysis and found it was lower in MHO than in MUO We are not aware of any studies that evaluated metabolic indicators of adipose tissue hypoxia, namely adipose tissue HIF1α protein content, in people with MHO and MUO.

In summary, currently there is not adequate evidence to conclude there is a physiologically important decrease in adipose tissue oxygenation in people with MUO compared with MHO. ECM remodeling and interstitial fibrosis.

The ECM of adipose tissue is composed of structural proteins primarily collagens I, III, IV, V, and VI and adhesion proteins fibronectin, elastin, laminin, and proteoglycans.

Compared with people who are lean, people with obesity have increased expression of genes for collagen I, IV, V, and VI and histological evidence of increased fibrosis, particularly pericellular fibrosis in omental adipose tissue and SAAT — In addition, we recently found that adipose tissue expression of connective tissue growth factor CTGF , a matricellular protein that regulates tissue fibrosis, is positively correlated with body fat mass and inversely correlated with indices of whole-body, liver, and skeletal muscle insulin sensitivity Adipose tissue expression of collagen genes and collagen content are also inversely correlated with insulin sensitivity in people with obesity, and decrease with weight loss , — These data support the notion that adipose tissue fibrosis is associated with MUO, as has been demonstrated in rodent models Immune cells and inflammation.

Obesity is typically associated with chronic, low-grade, noninfectious inflammation, which has been purported to be a cause of insulin resistance , It has been proposed that alterations in adipose tissue immune cells are an important cause of the chronic inflammation and insulin resistance associated with obesity , Macrophages are the most abundant immune cell in adipose tissue, and adipose tissue macrophage content is increased in people with obesity compared with people who are lean Moreover, adipose tissue macrophage content and crown-like structures macrophages surrounding an extracellular lipid droplet are greater in both SAAT and IAAT in people with MUO than in those with MHO; the increase in macrophage content is primarily due to an increase in M1-like proinflammatory macrophages 21 , — In conjunction with the alterations in adipose tissue immune cells, adipose tissue expression of inflammation-related genes is also greater in people with MUO than in those with MHO 21 , , , , , , but there is inconsistency in the specific genes that are upregulated among studies, and the differences in gene expression markers between MUO and MHO groups are often small 21 , , , , , Plasma concentrations of markers of inflammation, primarily C-reactive protein, plasminogen activator inhibitor-1 PAI-1 , IL-6, and TNF-α, are either higher in those with MUO than MHO 21 , 23 , 42 , 96 , — or not different between the two groups — The variability in results is likely related to the definitions used to identify MUO and MHO, the specific inflammatory markers evaluated in different studies, and the sample size needed for adequate statistical power because of small mean differences in plasma concentrations between groups.

The variability and small difference in adipose tissue expression of inflammatory markers in people with MHO and MUO and both the variability and small differences in plasma markers of inflammation between people with MUO and MHO question the importance of adipose tissue production and secretion of inflammatory cytokines in mediating the difference in systemic insulin resistance observed in people with MUO and MHO.

Nonetheless, it is possible that other immune cell—related mediators, such as adipose tissue macrophage-derived exosomes , are involved in the pathogenesis of metabolic dysfunction.

Lipolytic activity. Acute experimental increases in plasma free fatty acid FFA concentration, induced by infusion of a lipid emulsion, impair insulin-mediated suppression of hepatic glucose production and insulin-mediated stimulation of glucose disposal in a dose-dependent manner , However, the influence of endogenous adipose tissue lipolytic activity and plasma FFA concentration on insulin sensitivity in people with obesity is not clear because of conflicting results from different studies.

The importance of circulating FFA as a cause of insulin resistance in MUO is further questioned by studies that found no difference in basal, postprandial, and hour plasma FFA concentrations in people with obesity compared with those who are lean and more insulin sensitive , The reason s for the differences between studies are not clear, but could be related to the considerable individual day-to-day variability in FFA kinetics and plasma FFA concentration and differences in compensatory hyperinsulinemia and insulin-mediated suppression of adipose tissue lipolytic rate in people with insulin resistance , , Differences in the percentage of women between study cohorts will also affect the comparison of FFA kinetics and concentrations between MHO and MUO groups, because the rate of the appearance of FFA in the bloodstream in relationship to fat-free mass or resting energy expenditure is greater in women than in men , , yet muscle and liver , insulin sensitivity are greater in women.

Taken together, these studies suggest that differences in subcutaneous adipose tissue lipolytic activity do not explain the differences in insulin sensitivity between people with MHO and MUO. However, it is still possible that differences in lipolysis of IAAT and portal vein FFA concentration or differences in the effect of FFA on tissue muscle or liver insulin action contribute to the differences in insulin resistance between the two groups.

Adiponectin, the most abundant protein secreted by adipose tissue, is inversely associated with percentage body fat and directly associated with insulin sensitivity in both men and women Plasma adiponectin concentrations are often higher in people with MHO than MUO 12 , — The reasons for the lower adiponectin concentration in MUO than MHO are unclear but could be related to chronic hyperinsulinemia in people with MUO, which suppresses adipose tissue adiponectin production , , thereby generating a feed-forward cycle of decreased adiponectin secretion caused by insulin resistance and increased insulin resistance caused by decreased adiponectin secretion.

There is considerable heterogeneity in the metabolic complications associated with obesity. The risk of developing cardiometabolic diseases in people with obesity is directly related to the number and severity of metabolic abnormalities.

Accordingly, people with MHO are at lower risk of future T2D and CVD than people with MUO, but most people with MHO are at a higher risk than people who are MHL. However, people with MHO who do not have any metabolic abnormalities and remain MHO over time might not have an increased risk of developing cardiometabolic diseases compared with those who are MHL.

These findings support the need for a rigorous and universal definition of MHO proposed in Table 2 to allow reliable integration of data from different studies and facilitate research needed to identify the factor s involved in protecting some people with obesity from the adverse metabolic effects of excess adiposity.

The precise mechanisms responsible for preserved metabolic health in people with MHO are not known. The studies to date have not demonstrated important differences in lifestyle factors diet composition, physical activity, and sleep between MHO and MUO.

However, this does not mean that lifestyle is not an important regulator of metabolic health, but rather underscores the limitations in the assessment of lifestyle factors and in the definition of MHO in the current studies.

It is likely that there is an important genetic contribution to the metabolic phenotype in people with obesity. Although GWAS have identified genetic variants that are associated with increased adiposity in conjunction with a healthy metabolic profile , a better understanding of the genetic aspects of MHO will likely provide new insights into the mechanisms responsible for metabolic disease.

The influence of the gut microbiome on metabolic health is a rapidly emerging area of research. The potential for adverse and beneficial effects of the gut microbiome on metabolic health could be related to the composition and diversity of the microbiota and the ability of the gut barrier function to prevent leakage of bacteria and bacterial products across the intestine — In addition, studies conducted in human subjects demonstrate an increase in markers of inflammation and interstitial fibrosis in adipose tissue in people with MUO compared with MUO.

However, these studies are not able to determine whether these abnormalities are a cause or a consequence of insulin resistance and related metabolic dysfunction. The heterogeneity in the metabolic complications associated with obesity has important clinical implications, particularly in the current era of precision medicine and cost-effectiveness.

The classification of obesity by BMI status alone does not provide adequate insight into current health status, the potential risk of future adverse clinical outcomes, or who might benefit most from weight loss therapy.

The available data suggest that more intensive, and presumably more expensive, weight management therapies should be prioritized for those with MUO over those with MHO.

A, Trends Metaholic the prevalence of obesity, MUO, Cholesterol control tips MHO among US adults. B, Trends in Different types of onion bulbs proportion BMI for Metabolic Health MHO among US adults Healfh obesity. Obesity was defined BMI for Metabolic Health a body Merabolic Different types of onion bulbs of Mtabolic Among participants with obesity, MUO was defined as having any component of the metabolic syndrome waist circumference excluded and MHO was defined as meeting none of the metabolic syndrome criteria. In B, proportion estimates were age standardized to the nonpregnant adult population with obesity in the National Health and Nutrition Examination Survey cycles, using the same 3 age groups. Linear trends over time were evaluated using logistic regression.