And when the researchers compared those differences to the babies' adiposity then, they also found another clear pattern.
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Then, at or before age 10 or so, body fat increases in preparation for puberty – a phenomenon called adiposity rebound.
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This is why, according to Burtch, having high levels of Firmicutes is associated with obesity and high adiposity (fat storage).
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In children with obesity genes, "adiposity rebound occurs earlier and higher," said Dr. Daniel W. Belsky, an epidemiologist at Duke University School of Medicine.
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But even so, the correlation between relative inactivity and greater adiposity in these babies was noteworthy and could be worrisome, Dr. Benjamin-Neelon says.
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Beyond that, the risk of cardiovascular disease increased with B.M.I. With the four other measures of adiposity, the associations with cardiovascular disease risk were consistent even after controlling for other factors: As those measures increased, so did the risk for cardiovascular disease.
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DNA methylation in the introns of HIF3A is associated with BMI an adiposity.
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Conversely, serum resistin levels have been found to decline with decreased adiposity following medical treatment.
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ALDH1 is involved in the metabolism of Vitamin A. Animal models suggest that absence of the gene is associated with protection against visceral adiposity ().
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The effect of abdominal adiposity occurs not just in those who are obese, but also affects people who are non-obese and it also contributes to insulin sensitivity.
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Motorized transportation, social status, and adiposity: the China Health and Nutrition Survey. Qin L, Stolk RP, Corpeleijn E.Am J Prev Med. 2012 Jul;43(1):1-10. doi: 10.1016/j.amepre.2012.03.
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Much of what is hypothesized about a resistin role in energy metabolism and T2DM can be derived from studies showing strong correlations between resistin and obesity. The underlying belief among those in support of this theory is that serum resistin levels will increase with increased adiposity. Conversely, serum resistin levels have been found to decline with decreased adiposity following medical treatment. Specifically, central obesity (waistline adipose tissue) seems to be the foremost region of adipose tissue contributing to rising levels of serum resistin.
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Assumptions about the distribution between muscle mass and fat mass are inexact. BMI generally overestimates adiposity on those with more lean body mass (e.g., athletes) and underestimates excess adiposity on those with less lean body mass. A study in June 2008 by Romero-Corral et al. examined 13,601 subjects from the United States' third National Health and Nutrition Examination Survey (NHANES III) and found that BMI-defined obesity (BMI > 30) was present in 21% of men and 31% of women.
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Upon dysregulation of homeostasis in the adipose tissue, the decreased responses of ILC2s are a characteristic of obesity, as this interrupts their crucial role in energy homeostasis, resulting in reduced energy expenditure, and increased adiposity.
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Knockout studies in mice suggest that this subunit may play an important role in regulating energy balance and adiposity. The studies also suggest that this subunit may mediate the gene induction and cataleptic behavior induced by haloperidol.
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Concordantly, mice with selective Pikfyve gene disruption in skeletal muscle, the tissue mainly responsible for the decrease of postprandial blood sugar, exhibit systemic insulin resistance; glucose intolerance; hyperinsulinemia; and increased adiposity, i.e. symptoms, typical for human prediabetes.
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EP4 receptor-depleted mice exhibit slower weight gain; reduced adiposity upon high fat diet challenge; and shortened life span. These deficiencies are associated with disrupted lipid metabolism due to impaired triglyceride clearance; this impaired triglyceride clearance may underlie the cited deficiencies.
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Christensenella is a genus of non-spore-forming, anaerobic, and nonmotile bacteria from the family Christensenellaceae. The species C. minuta has been published and validated, and C. timonensis and C. massiliensis have been proposed as novel species of the genus Christensenella, all isolated from human feces. C. minuta in the gut has been associated with reduction in body weight and adiposity of mice.The human gut bacterium Christensenella minuta reduces weight and adiposity gains in mice, Jillian L. Waters, Julia K. Goodrich, Ruth E. Ley, Department of Molecular Biology and Genetics, Department of Microbiology, Cornell University Basic presentation of results.
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The inability of the β-cells to produce sufficient insulin in a condition of hyperglycemia is what characterizes the transition from insulin resistance to type 2 diabetes. Insulin resistance often is found in people with visceral adiposity, hypertension, hyperglycemia, and dyslipidemia involving elevated triglycerides, small dense low-density lipoprotein (sdLDL) particles, and decreased HDL cholesterol levels. With respect to visceral adiposity, a great deal of evidence suggests two strong links with insulin resistance. First, unlike subcutaneous adipose tissue, visceral adipose cells produce significant amounts of proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-a), and Interleukins-1 and −6, etc.
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Due to its association with insulin resistance, the risk of polycystic ovarian syndrome (PCOS) increases with adiposity. In the US approximately 60% of patients with PCOS have a BMI greater than 30. It remains uncertain whether PCOS contributes to obesity, or the reverse.
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Rats with a VMH lesion compared to normal rats overproduce a circulating satiety factor, to which the control rats can respond and rats with a VMH lesion cannot respond. A lesion to the VMH makes rats overproduce leptin, which they cannot respond to causing them to over eat, leading to obesity. Researchers looked at a series of twenty-one animals of various degrees of adiposity, with respect to growth appearance, fat distribution, general physical condition, and the correlation between the level of adiposity attained and the correlation of the hypothalamic lesion. Lesions in the hypothalamic area, particularly the region of the ventromedial hypothalamus interrupts a large number of the descending fibers from the hypothalamic cell groups that were found to contribute to obesity in rats.
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Obesity and diabetes are major healthcare problems globally. There is need for safe drugs for these metabolic diseases. In a mouse model of diet-induced obesity, ShK-186 counteracted the negative effects of increased caloric intake. It reduced weight gain, adiposity, and fatty liver; decreased blood levels of cholesterol, sugar, HbA1c, insulin, and leptin; and enhanced peripheral insulin sensitivity.
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There are 3 levels of consequences: physiologic, intermediate and clinical. The physiologic consequences contain hypoxia, sleep fragmentation, autonomic nervous system dysregulation or hyperoxia. The intermediate results regroup inflammation, pulmonary vasoconstriction, general metabolic dysfunction, oxidation of proteins and lipids or increased adiposity. The clinical repercussions are composed by pulmonary hypertension, accidents, obesity, diabetes, different heart diseases or hypertension.
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Body weight is regulated through energy balance, the amount of energy taken in versus the amount of energy expended over an extended period of time. Studies have shown that ghrelin levels are negatively correlated with weight. This data suggests that ghrelin functions as an adiposity signal, a messenger between the body's energy stores and the brain.
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Central obesity is a key feature of the syndrome, being both a sign and a cause, in that the increasing adiposity often reflected in high waist circumference may both result from and contribute to insulin resistance. However, despite the importance of obesity, affected people who are of normal weight may also be insulin-resistant and have the syndrome.
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D-leucine also terminates seizures in mice after the onset of seizure activity, at least as effectively as diazepam and without sedative effects. Decreased dietary intake of L-leucine promotes adiposity in mice. High blood levels of leucine are associated with insulin resistance in humans, mice, and rodents. This might be due to the effect of leucine to stimulate mTOR signaling.
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Dietary nutrient availability therefore modifies the ILC immune response to infection and inflammation, highlighting the importance of a balanced and healthy diet. ILC2s support a type- 2 immune environment in the adipose tissue, via the production of IL-5, IL-4 and IL-13. This regulates adiposity, insulin resistance, and caloric expenditure. Dysregulation of this causes persistent type 1 inflammation, leading to obesity.
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London: Little, Brown And Company. found that skin colour, skin homogeneity and facial adiposity (how fat is deposited around the face) all predict female attractiveness and therefore, mate preference. Skin tone has also been found to be an honest indicator of youthfulness and fertility;Fink, B., Grammer, K., & Thornhill, R. (2001). Human (Homo sapiens) facial attractiveness in relation to skin texture and color.
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In numerous experimental models, these proinflammatory cytokines disrupt normal insulin action in fat and muscle cells and may be a major factor in causing the whole-body insulin resistance observed in patients with visceral adiposity. Much of the attention on production of proinflammatory cytokines has focused on the IKK-beta/NF- kappa-B pathway, a protein network that enhances transcription of inflammatory markers and mediators that may cause insulin resistance. Second, visceral adiposity is related to an accumulation of fat in the liver, a condition known as non-alcoholic fatty liver disease (NAFLD). The result of NAFLD is an excessive release of free fatty acids into the bloodstream (due to increased lipolysis), and an increase in hepatic glycogenolysis and hepatic glucose production, both of which have the effect of exacerbating peripheral insulin resistance and increasing the likelihood of Type 2 diabetes mellitus.
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His first publications in 1920 and 1921 were clinical descriptions of aphasia and apraxia. His first scientific research paper, which was published in collaboration with P. Bailey from Cushing's laboratory, dealt with the neurogenic origin of diabetes insipidus. Bremer, together with Bailey, showed that a minimal lesion of the hypothalamus can induce experimental diabetes insipidus. These lesions were also shown to induce sleepiness and adiposity.
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Increased SMAD3 activity has, however, been implicated in the pathogenesis of scleroderma. SMAD3 is also a multifaceted regulator in adipose physiology and the pathogenesis of obesity and type 2 diabetes. SMAD3-knockout mice have diminished adiposity, with improved glucose tolerance and insulin sensitivity. Despite their reduced physical activity arising from muscle atrophy, these SMAD3-knockout mice are resistant to high- fat-diet induced obesity.
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Sam68-/- mice weighed less than Sam68+/+ littermates and magnetic resonance imaging analysis confirmed that young Sam68-/- mice exhibited a profound reduction in adiposity, although food intake was similar. Moreover, Sam68-/- mice were protected against dietary- induced obesity. Sam68 deficient preadipocytes (3T3-L1 cells) had impaired adipogenesis and Sam68-/- mice had ~45% less adult derived stem cells (ADSCs) in their stromal vascular fraction (SVF) from WAT.
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The body adiposity index (BAI) is a method of estimating the amount of body fat in humans. The BAI is calculated without using body weight, unlike the body mass index (BMI). Instead, it uses the size of the hips compared to the person's height. Based on population studies, the BAI is approximately equal to the percentage of body fat for adult men and women of differing ethnicities.
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Diabetic embryopathy refers to congenital maldevelopments that are linked to maternal diabetes. Prenatal exposure to hyperglycemia can result in spontaneous abortions, perinatal mortality, and malformations. Type 1 and Type 2 diabetic pregnancies both increase the risk of diabetes induced teratogenicity. The rate of congenital malformations is similar in Type 1 and 2 mothers because of increased adiposity and the age of women with type 2 diabetes.
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Tetradecylthioacetic acid (TTA) is a synthetic fatty acid used as a nutritional supplement. TTA acts as a peroxisome proliferator-activated receptor alpha (PPARα) agonist and increases mitochondrial fatty acid oxidation in vitro. In rodent studies, TTA has been reported to have other activities such as reducing inflammation and preventing high fat diet induced adiposity and insulin resistance. In human clinical study, there have been mixed observations in preliminary studies.
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In Britain, the weight at which people considered themselves to be overweight was significantly higher in 2007 than in 1999. These changes are believed to be due to increasing rates of adiposity leading to increased acceptance of extra body fat as being normal. Obesity is still seen as a sign of wealth and well-being in many parts of Africa. This has become particularly common since the HIV epidemic began.
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The BAI could be a good tool to measure adiposity due, at least in part, to the advantages over other more complex mechanical or electrical systems. Probably, the most important advantage of BAI over BMI is that weight is not needed. However, in general it seems that the BAI does not overcome the limitations of BMI.López AA, Cespedes ML, Vicente T, Tomas M, Bennasar-Veny M, et al.
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Subjects defined as TOFI have been described as being at higher risk of developing insulin resistance and type II diabetes due to the fact that they have reduced physical activity/VO2max, reduced insulin sensitivity, higher abdominal adiposity, and a more atherogenic lipid profile. Another important characteristic observed in this cohort is elevated levels of liver fat. It is shown that overconsumption of fructose can lead to TOFI by inducing inflammation associated cortisol release.
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Insulin resistance is a major feature of diabetes mellitus type 2 , and central obesity is correlated with both insulin resistance and T2DM itself. Increased adiposity (obesity) raises serum resistin levels, which in turn directly correlate to insulin resistance. Studies have also confirmed a direct correlation between resistin levels and T2DM. And it is waistline adipose tissue (central obesity) which seems to be the foremost type of fat deposits contributing to rising levels of serum resistin.
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Research identified dysregulated responses of ILC2s in adipose tissue as a factor in the development of obesity in mice since ILC2s also play important role in energy homeostasis. Methionine-enkephalin peptides produced by ILC2s act directly on adipocytes to upregulate UCP1 and promote emergence of beige adipocytes in white adipose tissue. Beige and brown adipose tissue are specialized in thermogenesis. The process of beiging leads to increased energy expenditure and decreased adiposity.
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One central aspect in the Ball School's dissemination is its system of basic and advanced training. Basic training refers to the Ball School's ABC (primary school children) and the Mini Ball School. Advanced training includes specific add-on programmes (advanced training in throwing games, in adiposity etc.). A participation in one of the Ball School's basic training requires a C-level trainer certification issued by a sports association as well as a minimum age of 16.
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Because of the commonalities between the two, rats may prove to be helpful in the search for the cause of human obesity. For example, in one experiment, male Sprague-Dawley rats were given either a low fat or a high fat diet, with the high fat diet containing 35% more fat than the low fat diet. The results of the study illustrate that the high fat diet rats had a higher adiposity index than the low fat diet rats.
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The number of adipocytes varies among different areas of the body, while their size varies according to the body's nutritional state. It acts as padding and as an energy reserve, as well as providing some minor thermoregulation via insulation. Subcutaneous fat is found just beneath the skin, as opposed to visceral fat, which is found in the peritoneal cavity, and can be measured using body fat calipers to give a rough estimate of total body adiposity.
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Diagnostic performance of body mass index to identify obesity as defined by body adiposity: a systematic review and metaanalysis. Int J Obes 2010 34(5): 791-9 Some studies have suggested that the main factor which explains the metabolic abnormalities in MONW individuals is fat distribution. On the basis of these studies, a scoring method has been proposed to identify MONW individuals, based on the presence of associated diseases or biochemical abnormalities related to insulin resistance.
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Obesity during pregnancy and high-fat maternal diets both show strong associations with obesity in offspring. As the number of overweight reproductive-age women increases, the number of overweight children and infants also increases. It has been postulated that maternal obesity causes an accumulation of fat in fetal adipose tissue (adiposity) and predisposes babies for obesity in childhood and adulthood. Animal studies have shown that maternal overnutrition may impact brain development and cause disruptions to programming of the hypothalamus.
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Jako has permanent truncal adiposity (a collection of fat at the waist, back and neck, and wasting in the extremities.) She experiences dangerously elevated lipid levels, both cholesterol and triglycerides due to side effects from her medications. The elevated lipids required the addition of Gemfibrozil to control them. While a treatment advocate, Jako emphasizes the need for patient education and a holistic approach. Her long term success on one three drug combination or HAART is the result of perfect adherence since 1997.
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Overnight worker––who had lower insulin sensitivity and increased adiposity from disrupted hemostasis––exhibited a slow postprandial increase in their anorexigenic xenin level, while a suppression in their orexigenic ghrelin level. Xenin promotes insulin release by gastric inhibitory polypetide to regulate glucose homeostasis. Its increase of insulin secretion is indirect and would not produce any effects by itself. Xenin's effect on insulin increase is not observed in type 2 diabetes patients when using a dosage of 4 pmol ⋅kg−1⋅min−1.
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Children with obstructive sleep- disordered breathing also show a faster heart rate during wakefulness and during sleep. In adult patients, OSA has been shown to be associated with insulin resistance. In children, metabolic consequences of OSA are complicated to assess as they can also be associated to puberty and/or obesity (if present). However, when OSA is associated with obesity, the interaction of the two conditions can lead to metabolic disturbances such as insulin resistance and altered lipidemia, liver disease, abdominal adiposity and metabolic syndrome.
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Janda demonstrated that one could manipulate the immune system to generate antibodies against cocaine. He has demonstrated that antibodies resulting from this approach can protect from the lethal effects of cocaine overdose, even when administered after cocaine exposure. Recently, he detailed the treatment of cocaine addiction with viruses. Janda and colleagues then showed that an active vaccine against the orexigenic hormone ghrelin can slow the rate of weight gain, and adiposity, and do this through an entirely metabolic mechanism, as food intake was unchanged.
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Some other studies have pointed out that for people of Asian descent and without diabetes, their insulin resistance levels are higher than non- diabetic people of Caucasian descent. Thus, Asian Americans are relatively more predisposed to develop type 2 diabetes. This suggests that insulin resistance, rather than body mass index (BMI) should be targeted while making diagnoses. A potential biomarker to identify diabetes in young Asian American population is adipocyte fatty acid binding protein that has a strong association with insulin resistance but is independent of adiposity.
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The key sign of metabolic syndrome is central obesity, also known as visceral, male-pattern or apple-shaped adiposity. It is characterized by adipose tissue accumulation predominantly around the waist and trunk. Other signs of metabolic syndrome include high blood pressure, decreased fasting serum HDL cholesterol, elevated fasting serum triglyceride level, impaired fasting glucose, insulin resistance, or prediabetes. Associated conditions include hyperuricemia; fatty liver (especially in concurrent obesity) progressing to nonalcoholic fatty liver disease; polycystic ovarian syndrome in women and erectile dysfunction in men; and acanthosis nigricans.
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Research into the adipose-derived hormones adiponectin and resistin is ongoing. Like leptin, these hormones also affect energy balance and metabolism. Like leptin, observations in both humans and animal models have shown that adiponectin is relevant to insulin sensitivity and energy homeostasis. In contrast, the relationship between resistin and adiposity is not consistent between rodent models and human subjects (See Peter Arner, 2005: "Resistin: yet another adipokine tells us that men are not mice"); hence, the notion of resistin as a genuine adipose-derived hormone remains questionable.
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ILC2s promote the beiging of adipocytes, and therefore increased energy expenditure. Therefore, decreased responses of ILC2s in the tissue are a characteristic of obesity, as this interrupts their crucial role in energy homeostasis, resulting in reduced energy expenditure and increased adiposity. In addition to ILC2s, ILC1s contribute to the homeostasis of adipose tissue macrophages in both lean and obese conditions, making up 5-10% of the resident lymphocyte population, in human lean adipose depots. A high fat diet increases ILC1 number, and activation of adipose tissue, increasing IFN-γ and TNF-α levels.
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A study in Chinese young adults indicates a strong relationship between serum FABP1 levels and lipid profile, body measurements and homeostatic parameters. Increased BMI and insulin resistance in subjects demonstrated higher serum FABP1 with a particular correlation in subjects with central adiposity. This elevation is suggested to occur as a compensatory up-regulation of the protein in an attempt to counter the high metabolic stress associated with obesity. Alternately obesity may in fact lead the human body to develop resistance to the actions of FABP1 leading to the compensatory up-regulation.
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Obesity, or more specifically, adiposity or fatness, has also been linked to an increasing incidence of tendinopathy. The most commonly accepted cause for this condition however is seen to be an overuse syndrome in combination with intrinsic and extrinsic factors leading to what may be seen as a progressive interference or the failing of the innate healing response. Tendinopathy involves cellular apoptosis, matrix disorganization and neovascularization. Classic characteristics of "tendinosis" include degenerative changes in the collagenous matrix, hypercellularity, hypervascularity, and a lack of inflammatory cells which has challenged the original misnomer "tendinitis".
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Many children born small for gestational age (SGA) because of intrauterine growth restriction (IUGR) have an earlier onset of adrenarche, which raises the possibility that timing of adrenarche may be affected by physiological programming in infancy. Adrenarche also occurs prematurely in many children who are overweight, suggesting a possible relationship with body mass or adiposity signals. The principal physical consequences of adrenarche are androgen effects, especially pubic hair (in which Tanner stage 2 becomes Tanner stage 3) and the change of sweat composition that produces adult body odor. Increased oiliness of the skin and hair and mild acne may occur.
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Isoleucine, like other branched-chain amino acids, is associated with insulin resistance: higher levels of isoleucine are observed in the blood of diabetic mice, rats, and humans. Mice fed an isoleucine deprivation diet for one day have improved insulin sensitivity, and feeding of an isoleucine deprivation diet for one week significantly decreases blood glucose levels. In diet-induced obese and insulin resistant mice, a diet with decreased levels of isoleucine and the other branched-chain amino acids results in reduced adiposity and improved insulin sensitivity. In humans, a protein restricted diet lowers blood levels of isoleucine and decreases fasting blood glucose levels.
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This fact takes on significant implications considering the well understood link between central obesity and insulin resistance, two marked peculiarities of T2DM. Although it seems that resistin levels increase with obesity, can we conclude then that such serum resistin increases are accountable for the insulin resistance that appears to be associated with increased adiposity? Many researchers in their respective studies have shown that this is indeed the case by finding positive correlations between resistin levels and insulin resistance. This discovery is further supported by studies that confirm a direct correlation between resistin levels and subjects with T2DM.
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The BMI is generally used as a means of correlation between groups related by general mass and can serve as a vague means of estimating adiposity. The duality of the BMI is that, while it is easy to use as a general calculation, it is limited as to how accurate and pertinent the data obtained from it can be. Generally, the index is suitable for recognizing trends within sedentary or overweight individuals because there is a smaller margin of error. The BMI has been used by the WHO as the standard for recording obesity statistics since the early 1980s.
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CMA is important in regulating cellular metabolism. Specific depletion of CMA in liver results in robust hepatic glycogen use accompanied with accumulation of fat in the liver, along with altered glucose homeostasis, increased energy expenditure and reduced peripheral adiposity. Proteomics analyses identified several enzymes of the carbohydrate and the lipid metabolism pathways to be CMA substrates, and their altered degradation in the knockout mice explaining the abnormal metabolic phenotype of the CMA-deficient mice. CMA activity has been shown to be modulated through retinoic acid receptor alpha signaling and is specifically activated by designed all-trans retinoic acid derivatives in cultured cells.
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About 240,000 tonnes of crystalline fructose are produced annually.Wolfgang Wach "Fructose" in Ullmann’s Encyclopedia of Industrial Chemistry 2004, Wiley-VCH, Weinheim. Excessive consumption of fructose (especially from sugar-sweetened beverages) may contribute to insulin resistance, obesity, elevated LDL cholesterol and triglycerides, leading to metabolic syndrome. The European Food Safety Authority stated that fructose may be preferable over sucrose and glucose in sugar-sweetened foods and beverages because of its lower effect on postprandial blood sugar levels, and noted that "high intakes of fructose may lead to metabolic complications such as dyslipidaemia, insulin resistance, and increased visceral adiposity".
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Obese rats showed significant increases in weight gain, adipose tissue mass, and adiposity and atherogenic indices, and presented glucose intolerance, insulin resistance, dyslipidaemia, and hepatic steatosis. Botryosphaeran significantly reduces feed intake, weight gains, periepididymal and mesenteric fat, and improves glucose tolerance in obese rats. Botryosphaeran, furthermore, reduces the serum levels of triglyceride and VLDL-cholesterol, and increased HDL-cholesterol and glycogen in liver, and reduces the atherogenic index. The above data demonstrated the beneficial effects of botryosphaeran in reducing the stimulatory effect of obesity on dyslipidaemia and hepatic steatosis, and can play a potential role in the management of obesity comorbidities.
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Further studies have examined the epigenetic changes resulting from a high protein/low carbohydrate diet during pregnancy. This diet caused epigenetic changes that were associated with higher blood pressure, higher cortisol levels, and a heightened Hypothalamic-pituitary-adrenal (HPA) axis response to stress. Increased methylation in the 11β-hydroxysteroid dehydrogenase type 2 (HSD2), glucocorticoid receptor (GR), and H19 ICR were positively correlated with adiposity and blood pressure in adulthood. Glucocorticoids play a vital role in tissue development and maturation as well as having effects on metabolism. Glucocorticoids’ access to GR is regulated by HSD1 and HSD2.
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Recent research indicates prolonged chronic stress can contribute to metabolic syndrome by disrupting the hormonal balance of the hypothalamic-pituitary-adrenal axis (HPA-axis). A dysfunctional HPA-axis causes high cortisol levels to circulate, which results in raising glucose and insulin levels, which in turn cause insulin-mediated effects on adipose tissue, ultimately promoting visceral adiposity, insulin resistance, dyslipidemia and hypertension, with direct effects on the bone, causing "low turnover" osteoporosis. HPA-axis dysfunction may explain the reported risk indication of abdominal obesity to cardiovascular disease (CVD), type 2 diabetes and stroke. Psychosocial stress is also linked to heart disease.
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A large central adiposity deposit has been assigned many common use names, including; “spare tire”, “tummy”, “gut”, “paunch” and “pot belly” among others. Several colloquial terms used to refer to central obesity, and to people who have it, refer to beer drinking. However, there is little scientific evidence that beer drinkers are more prone to central obesity, despite its being known colloquially as "beer belly", "beer gut", or "beer pot". One of the few studies conducted on the subject did not find that beer drinkers are more prone to central obesity than nondrinkers or drinkers of wine or spirits.
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The higher amount of Firmicutes was also linked to more adiposity and body weight within mice. Specifically, within obese mice, the class Mollicutes (within the Firmicutes phylum) was the most common. When the microbiota of obese mice with this higher Firmicutes abundance was transplanted into the guts of germ-free mice, the germ-free mice gained a significant amount of fat as compared to those transplanted with the microbiota of lean mice with lower Firmicutes abundance. The presence of Christensenella (Firmicutes, in class Clostridia), isolated from human faeces, has been found to correlate with lower body mass index.
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Valine, like other branched-chain amino acids, is associated with insulin resistance: higher levels of valine are observed in the blood of diabetic mice, rats, and humans. Mice fed a valine deprivation diet for one day have improved insulin sensitivity, and feeding of a valine deprivation diet for one week significantly decreases blood glucose levels. In diet-induced obese and insulin resistant mice, a diet with decreased levels of valine and the other branched-chain amino acids results in reduced adiposity and improved insulin sensitivity. The valine catabolite 3-hydroxyisobutyrate promotes skeletal muscle insulin resistance in mice by stimulating fatty acid uptake into muscle and lipid accumulation.
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The amount of evidence supporting the resistin link theory between obesity and T2DM is vast. Nevertheless, this theory lacks support from the entire scientific community, as the number of studies presenting evidence against it continues to expand. Such studies have found significantly decreased serum concentrations of resistin with increased adiposity, suggesting not only that resistin is downregulated in obese subjects, but also that decreased resistin levels may contribute to the links between obesity and T2DM. Data contradicting the idea that weight loss coincides with decreased serum resistin concentrations have also been presented; such studies instead report that weight loss is associated with marked increases in serum resistin.
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Exposure to social stress in childhood can also have long-term effects, increasing risk for developing diseases later in life. In particular, adults who were maltreated (emotionally, physically, sexually abused or neglected) as children report more disease outcomes, such as stroke, heart attack, diabetes, and hypertension or greater severity of those outcomes. The Adverse Childhood Experiences study (ACE), which includes over seventeen thousand adults, also found that there was a 20% increase in likelihood for experiencing heart disease for each kind of chronic familial social stressor experienced in childhood, and this was not due to typical risk factors for heart disease such as demographics, smoking, exercise, adiposity, diabetes, or hypertension.
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Regarding drug therapies, it has been stated that: "An emerging concept is that the development of anti-obesity agents must not only reduce fat mass (adiposity) but must also correct fat dysfunction (adiposopathy)." This is in recognition that the use of weight loss therapies and drugs in overweight patients must not only improve the weight of patients, but must also improve the health of patients. Unfortunately, not everyone understands the central role that sick fat plays in the development of metabolic disease. This is partly because in the past, most of the attention of what causes metabolic disease was given to other body organs.
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Monounsaturated fatty acids, the products of SCD-1 catalyzed reactions, can serve as substrates for the synthesis of various kinds of lipids, including phospholipids, triglycerides, and can also be used as mediators in signal transduction and differentiation. Because MUFAs are heavily utilized in cellular processes, variation in SCD activity in mammals is expected to influence physiological variables, including cellular differentiation, insulin sensitivity, metabolic syndrome, atherosclerosis, cancer, and obesity. SCD-1 deficiency results in reduced adiposity, increased insulin sensitivity, and resistance to diet-induced obesity. Under non-fasting conditions, SCD-1 mRNA is highly expressed in white adipose tissue, brown adipose tissue, and the Harderian gland.
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Studies have looked at the effects on fat oxidation and other metabolic responses when replacing sugars with isomaltulose in meals (or drinks) taken by healthy or overweight to obese adults, with or without impaired glucose tolerance, while largely sedentary. These studies have shown isomaltulose to have a role in reducing adiposity, at least central obesity. Abdominal fat decreases when consuming isomaltulose instead of sucrose (sugar replacement) or instead of breakfast calories (largely carbohydrate replacement). This is brought about at least in part by a lower GIP and higher GLP-1 response when carbohydrate is slow to digest and is absorbed slowly in the lower (distal) small intestine.
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A systematic examination of reviews, published in 2019, concluded that evidence, although of mainly low to moderate quality, showed an association of screen time with a variety of health problems including: "adiposity, unhealthy diet, depressive symptoms and quality of life". They also concluded that moderate use of digital media may have benefits for young people in terms of social integration, a curvilinear relationship found with both depressive symptoms and overall well-being. A research study done on urban adolescents in China revealed that more than a quarter of adolescents in China were exposed to over 2 hours of screen time per day. They found that screen time and physical activity was independently associated with mental health.
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Historian Susan Maclean Kybett ascribes his demise to scurvy, which is caused by insufficient vitamin C most often due to a lack of fresh fruits and vegetables in ones diet. Alternatively, his wives' pattern of pregnancies and his mental deterioration have led some to suggest that he may have been Kell positive and suffered from McLeod syndrome. According to another study, Henry's history and body morphology may have been the result of traumatic brain injury after his 1536 jousting accident, which in turn led to a neuroendocrine cause of his obesity. This analysis identifies growth hormone deficiency (GHD) as the reason for his increased adiposity but also significant behavioural changes noted in his later years, including his multiple marriages.
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Excessive fat in the crest of the neck, and areas of the shoulder and flank, are suggestive of EMS EMS horses tend to become obese very easily, depositing fat in the crest, shoulders, loin, above the eyes, around the tail head, and the mammary glands or prepuce, even when the rest of the body appears to be in normal condition. Some horses may have regional adiposity, and others may even appear normal weight, so obesity is not a definitive clinical sign of a horse with EMS. Horses will be insulin resistant (IR), and may have hyperinsulinemia, have abnormal blood glucose, or abnormal insulin responses to glucose. IR predisposes the animal to laminitis, and horses with EMS may have had previous episodes in their history.
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DXA scans can also be used to measure total body composition and fat content with a high degree of accuracy comparable to hydrostatic weighing with a few important caveats. From the DXA scans, a low resolution "fat shadow" image can also be generated, which gives an overall impression of fat distribution throughout the body It has been suggested that, while very accurately measuring minerals and lean soft tissue (LST), DXA may provide skewed results due to its method of indirectly calculating fat mass by subtracting it from the LST and/or body cell mass (BCM) that DXA actually measures. DXA scans have been suggested as useful tools to diagnose conditions with an abnormal fat distribution, such as familial partial lipodystrophy, but its use in this context is yet to be FDA approved. They are also used to assess adiposity in children, especially to conduct clinical research.
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In IL-33 knockout mice, it was discovered that nuclear IL-33 is associated with wound healing as mice without the protein healed significantly slower than mice with the IL-33 protein. Elevated levels of IL-33 are associated with asthma. In mice, IL-33 was found to effect the production of methionine- enkephalin peptides in group 2 innate lymphocytes, in turn promoting the emergence of beige adipocytes, which leads to increased energy expenditure and decreased adiposity. Elevated levels of IL-33 have been reported in some patients with nonsmall cell lung carcinomas. The source of elevated serum levels of IL-33 during the early stages could be bronchial and vascular epithelium. IL-33 knockdown showed lower growth of nonsmall cell lung carcinomas, while overexpression of IL-33 resulted in increased growth. Blocking of IL-33 reduced the growth of human nonsmall cell lung carcinomas. I mice model blocking of IL-33 inhibited tumor growth in immunodeficient mice. In the mouse colon carcinoma model, IL-33 was expressed by tumor stromal cells, while the colon carcinoma cells did not express ST2 with or without IL-33 stimulation.
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In accordance, a 2009 study found that an aromatase inhibitor had no effect on the estrogenic potencies of tibolone or its metabolites in vitro, unlike the case of testosterone. In addition, another 2009 study found that the estrogenic effects of tibolone on adiposity in rats do not require aromatization (as indicated by the use of aromatase knockout mice), further in support that 3α-hydroxytibolone and 3β-hydroxytibolone are indeed responsible for such effects. These findings are also in accordance with the fact that tibolone decreases sex hormone-binding globulin (SHBG) levels by 50% in women and does not increase the risk of venous thromboembolism (VTE) ( = 0.92), which would not be expected if the medication formed a potent, liver metabolism-resistant estrogen similar to ethinylestradiol in important quantities. (For comparison, combined oral contraceptives containing ethinylestradiol, due mostly or completely to the estrogen component, have been found to increase SHBG levels by 200 to 400% and to increase the risk of VTE by about 4-fold ( = 4.03).) In spite of the preceding, others have held, as recently as 2011, that tibolone is converted into 7α-methylethinylestradiol in small quantities.
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