The Association between Adult Weight Gain and Insulin Resistance at Middle Age: Mediation by Visceral Fat and Liver Fat.
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ABSTRACT:
SUBMITTER: Verkouter I
PROVIDER: S-EPMC6832997 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:To investigate visceral fat accumulation and markers of insulin resistance in relation to elevated depressive symptoms (EDS).Participants were 4,333 male employees (mean age, 49.3 years) who underwent abdominal computed tomography scanning, measured fasting insulin, and did not self-report diabetes and mental disorders under treatment and history of cancer, myocardial infarction, and stroke. Multivariable logistic regression was used to assess the association of EDS with abdominal fat deposition and markers of insulin resistance.Visceral fat area (VFA) and fasting insulin were significantly, positively associated with EDS. Multivariable-adjusted odds ratios (95% confidence interval) of high VFA for the lowest through highest quartile of depression score were 1 (reference), 1.18 (0.97-1.42), 1.25 (1.02-1.54), 1.23 (1.01-1.51), respectively, and corresponding figures for high fasting insulin were 1 (reference), 0.98 (0.80-1.19), 1.12 (0.91-1.38), and 1.29 (1.06-1.57), respectively. Subcutaneous fat area was not associated with EDS.Results suggest that EDS is related to visceral, but not subcutaneous, fat accumulation and insulin resistance in middle-aged Japanese men.
| S-EPMC4758729 | biostudies-other
Project description:To evaluate the cross-sectional relationship between migraine and pregravid obesity; and to assess the risk of adult weight gain among women with history of a pediatric diagnosis of migraine.Obesity, comorbid with pain disorders including migraine, shares common pathophysiological characteristics including systemic inflammation, and derangements in adipose-tissue derived cytokines. Despite biochemical and epidemiological commonalities, obesity-migraine associations have been inconsistently observed.A cohort of 3733 women was interviewed during early pregnancy. We ascertained participants' self-reported history of physician-diagnosed migraine and collected self-reported information about pregravid weight, adult height, and net weight change from age 18 to the 3-months period before pregnancy. Using pregravid body mass index, we categorized participants as follows: lean (< 18.5 kg/m²), normal (18.5-24.9 kg/m²), overweight (25-29.9 kg/m²), obese (30-34.9 kg/m²), severely obese (35-39.9 kg/m²), and morbidly obese (? 40 kg/m²). Logistic regression procedures were used to estimate odds ratios (ORs) and 95% confidence intervals (CIs).After adjusting for confounders, relative to normal weight women, obese women had a 1.48-fold increased odds of migraine (OR = 1.48; 95% CI 1.12-1.96). Severely obese (OR = 2.07; 95% CI 1.27-3.39) and morbidly obese (OR = 2.75; 95% CI 1.60-4.70) had the highest odds of migraines. Women with a history of diagnosed pediatric migraine had a 1.67-fold higher odds of gaining ? 10.0 kg above their weight at age 18, as compared with non-migraineurs (OR = 1.67; 95% CI 1.13-2.47).These data support earlier observations of migraine-obesity association among women, and extend the literature to include evidence of adult weight gain among women with a history of pediatric migraine.
| S-EPMC3187699 | biostudies-literature
Project description:BackgroundIt is unclear to what extent adherence to dietary guidelines may specifically affect visceral fat and liver fat. We aimed to study the association between the Dutch Healthy Diet Index (DHD-index) and total body fat, visceral adipose tissue (VAT) and hepatic triglyceride content (HTGC) in middle-aged men and women.DesignIn this cross-sectional study, VAT was assessed by magnetic resonance imaging (MRI) in 2580 participants, and HTGC by proton-MR spectroscopy in 2083 participants. Habitual dietary intake and physical activity were estimated by questionnaire. Adherence to the current Dutch dietary guidelines was estimated by the 2015 DHD-index score based on the thirteen components (vegetables, fruit, wholegrain products, legumes, nuts, dairy, fish, tea, liquid fats, red meat, processed meat, sweetened beverages, and alcohol). The DHD-index ranges between 0 and 130 with a higher score indicating a healthier diet. We used linear regression to examine associations of the DHD-index with VAT and HTGC, adjusted for age, smoking, education, ethnicity, basal metabolic rate, energy restricted diet, menopausal state, physical activity, total energy intake, and total body fat. We additionally excluded the components one by one to examine individual contributions to the associations.ResultsIncluded participants (43% men) had a mean (SD) age of 56 (6) years and DHD-index score of 71 (15). A 10-point higher DHD-index score was associated with 2.3 cm2 less visceral fat (95% CI; -3.5; -1.0 cm2) and less liver fat (0.94 times, 95% CI; 0.90; 0.98). Of all components, exclusion of dairy attenuated the associations with TBF and VAT.ConclusionsAdherence to the dietary guidelines as estimated by the DHD-index was associated with less total body fat, and with less visceral and liver fat after adjustment for total body fat. These findings might contribute to better understanding of the mechanisms underlying associations between dietary habits and cardiometabolic diseases.
| S-EPMC6997120 | biostudies-literature
Project description:Metabolic-associated fatty liver disease is a major cause of chronic pathologies, of which maternal obesity is a frequent risk factor. Gut wall and microbiota, visceral fat, and liver form a pre-systemic network for substrates and pro-inflammatory factors entering the body, undergoing accelerated maturation in early-life when the weaning reaction, i.e., a transitory inflammatory condition, affects lifelong health. We aimed to characterize organ metabolism in the above network, in relation to weaning reaction and maternal obesity. Weaning or 6-months-old offspring of high-fat-diet and normal-diet fed dams underwent in vivo imaging of pre-/post-systemic glucose uptake and tissue radiodensity in the liver, visceral fat, and intestine, a liver histology, and microbiota and metabolic pathway analyses. Weaning mice showed the dominance of gut Clostridia and Bacteroidia members, overexpressing pathways of tissue replication and inflammation; adulthood increased proneness to steatohepatitis, and Desulfovibrio and RF39 bacteria, and lipopolysaccharide, bile acid, glycosaminoglycan, and sphingolipid metabolic pathways. In vivo imaging could track organ maturation, liver inflammation, and protective responses. A maternal high-fat diet amplified the weaning reaction, elevating liver glucose uptake, triglyceride levels, and steatohepatitis susceptibility along the lifespan. The visceral network establishes a balance between metabolism and inflammation, with clear imaging biomarkers, and crucial modulation in the weaning time window.
| S-EPMC8541006 | biostudies-literature
Project description:Loss of liver fatty acid binding protein (L-FABP) decreases long chain fatty acid uptake and oxidation in primary hepatocytes and in vivo. On this basis, L-FABP gene ablation would potentiate high-fat diet-induced weight gain and weight gain/energy intake. While this was indeed the case when L-FABP null (-/-) mice on the C57BL/6NCr background were pair-fed a high-fat diet, whether this would also be observed under high-fat diet fed ad libitum was not known. Therefore, this possibility was examined in female L-FABP (-/-) mice on the same background. L-FABP (-/-) mice consumed equal amounts of defined high-fat or isocaloric control diets fed ad libitum. However, on the ad libitum-fed high-fat diet the L-FABP (-/-) mice exhibited: (1) decreased hepatic long chain fatty acid (LCFA) β-oxidation as indicated by lower serum β-hydroxybutyrate level; (2) decreased hepatic protein levels of key enzymes mitochondrial (rate limiting carnitine palmitoyl acyltransferase A1, CPT1A; HMG-CoA synthase) and peroxisomal (acyl CoA oxidase 1, ACOX1) LCFA β-oxidation; (3) increased fat tissue mass (FTM) and FTM/energy intake to the greatest extent; and (4) exacerbated body weight gain, weight gain/energy intake, liver weight, and liver weight/body weight to the greatest extent. Taken together, these findings showed that L-FABP gene-ablation exacerbated diet-induced weight gain and fat tissue mass gain in mice fed high-fat diet ad libitum--consistent with the known biochemistry and cell biology of L-FABP.
| S-EPMC3640860 | biostudies-literature
Project description:Importance: The association of weight gain from early to middle adulthood with disease risk has not been adequately studied.Objective: To investigate the association of adult weight gain with major health outcomes in a Chinese population with low body weight in early adulthood.Design, setting, and participants: This population-based cohort study assessed data from 48?377 women and 35?989 men aged 40 to 59 years at recruitment in 2 prospective cohort studies in China. The Shanghai Women's Health Study recruited 74?941 women, aged 40 to 70 years, from January 1, 1996, to December 31, 2000, and the Shanghai Men's Health Study recruited 61?482 men, aged 40 to 74 years, from January 1, 2002, to December 31, 2006. This analysis was conducted from September 1, 2017, to April 30, 2018.Exposures: Weight gain from 20 years of age to 40 to 59 years of age.Main outcomes and measures: Mortality and incidence of cancers and other chronic diseases.Results: This analysis included 48?377 women (mean [SD] age, 47.8 [5.3] years) and 35?989 men (mean [SD] age, 49.6 [5.1] years). Per 5-kg weight gain from early to middle adulthood was associated with an approximately 10% (hazard ratio [HR], 1.09; 95% CI, 1.04-1.14 for men; HR, 1.14; 95% CI, 1.11-1.19 for women) elevated all-cause mortality and a greater than 20% (HR, 1.26; 95% CI, 1.16-1.38 for men; HR, 1.23; 95% CI, 1.14-1.33 for women) cardiovascular disease-related mortality in later life among individuals who reached a body mass index (BMI) of 23 or higher at middle adulthood. Body mass index at middle adulthood also modified the association of weight gain with risk of obesity-related cancers, with weight gain of 20 kg or more associated with increased risks both for men (HR, 1.34; 95% CI, 1.07-1.67) and for women (HR 1.45; 95% CI, 1.24-1.68). No similar associations were found for individuals with a BMI of 18.5 to 22.9. Regardless of BMI, weight gain was associated with elevated risks of type 2 diabetes, hypertension, fatty liver disease, stroke, gout, and gallstones, particularly for type 2 diabetes (HR, 7.87; 95% CI, 6.91-8.97 for women; HR, 4.95; 95% CI, 4.23-5.79 for men) and fatty liver disease (HR, 3.68; 95% CI, 3.42-3.95 for women; HR, 2.83, 95% CI, 2.56-3.13 for men) in individuals with weight gain of 20 kg or more compared with those with a healthy weight.Conclusions and relevance: This study found that weight gain from early to middle adulthood was associated with disease incidence and mortality in later life. The BMI at middle adulthood modified the association of weight gain with mortality and cancer incidence but not risk of other major chronic diseases.
| S-EPMC6991199 | biostudies-literature
Project description:(1) Background: We previously demonstrated that disruption of IP6K1 improves metabolism, protecting mice from high-fat diet-induced obesity, insulin resistance, and non-alcoholic fatty liver disease and steatohepatitis. Age-induced metabolic dysfunction is a major risk factor for metabolic diseases. The involvement of IP6K1 in this process is unknown. (2) Methods: Here, we compared body and fat mass, insulin sensitivity, energy expenditure and serum-, adipose tissue- and liver-metabolic parameters of chow-fed, aged, wild type (aWT) and whole body Ip6k1 knockout (aKO) mice. (3) Results: IP6K1 was upregulated in the adipose tissue and liver of aWT mice compared to young WT mice. Moreover, Ip6k1 deletion blocked age-induced increase in body- and fat-weight and insulin resistance in mice. aKO mice oxidized carbohydrates more efficiently. The knockouts displayed reduced levels of serum insulin, triglycerides, and non-esterified fatty acids. Ip6k1 deletion partly protected age-induced decline of the thermogenic uncoupling protein UCP1 in inguinal white adipose tissue. Targets inhibited by IP6K1 activity such as the insulin sensitivity- and energy expenditure-inducing protein kinases, protein kinase B (PKB/Akt) and AMP-activated protein kinase (AMPK), were activated in the adipose tissue and liver of aKO mice. (4) Conclusions: Ip6k1 deletion maintains healthy metabolism in aging and thus, targeting this kinase may delay the development of age-induced metabolic dysfunction.
| S-EPMC8878859 | biostudies-literature
Project description:Permethrin is a pyrethroid pesticide that was previously reported to promote fat accumulation and insulin resistance in vitro. A recent study in female mice also found that permethrin could promote high fat-induced insulin resistance. The effects of permethrin on glucose and lipid metabolisms in male mice, however, remain unknown. The purpose of this study was to investigate the effects and interactions of permethrin exposure (50, 500, and 5000 μg/kg body weight/day) and dietary fat (low fat, 4% w/w; high fat, 20% w/w) on development of obesity and insulin resistance in male C57BL/6J mice. Our results showed that permethrin treatment significantly increased body weight, fat mass, and insulin resistance with high fat diet, but not with low fat diet, without influencing energy intake. Permethrin treatment also significantly increased serum levels of insulin, glucose, leptin, triglycerides and cholesterol. Further results showed that permethrin inhibited AMP-activated protein kinase in white adipose tissue. These results suggest that permethrin interacts with dietary fat to alter lipid and glucose metabolisms in male C57BL/6J mice.
| S-EPMC5756676 | biostudies-literature
Project description:ObjectiveAcross two studies, we examine if the relationships between perceived weight stigma, maladaptive eating behaviors (Study 1 & 2) and weight gain (Study 2) are mediated by fear of fat (FOF).MethodIn Study 1, 189 participants completed measures of eating behavior (e.g., emotional and restrained eating), FOF, perceived weight stigma and height and weight. In Study 2, a longitudinal design, participants reported their perceived weight stigma, FOF and had their height and weight measured; they then returned 10 weeks later to complete measures of eating behaviors (e.g., flexible restraint, ridged restraint, and emotional eating) and height and weight. We examined the predictive value of weight stigma at session 1 on eating behavior and weight gain at session 2. Further, we examined FOF as a mediator of these relationships.ResultsIn Study 1, we found that FOF significantly mediated the positive relationship between perceived weight stigma and restrained eating behavior (b=.13, CI: .09 to .19). In Study 2, we found that perceived weight stigma predicted weight gain over the 10-week period and that this relationship was mediated by both FOF (b=.31, CI: .03 to .78) and rigid restraint of eating (b=.07, CI: .002 to .28). Flexible restraint and emotional eating behavior were not mediators of the relationship between perceived weight stigma and weight gain.ConclusionFear of fat may be one process through which perceptions of weight stigma lead to maladaptive eating behavior and weight gain. Understanding this important process may lead to more effective healthy weight interventions.
| S-EPMC6132275 | biostudies-literature
Project description:IntoductionExcess visceral and liver fat are known risk factors for cardiometabolic disorders. Metabolomics might allow for easier quantification of these ectopic fat depots, instead of using invasive and costly tools such as MRI or approximations such as waist circumference.ObjectiveWe explored the potential use of plasma metabolites as biomarkers of visceral adipose tissue (VAT) and hepatic triglyceride content (HTGC).MethodsWe performed a cross-sectional analysis of a subset of the Netherlands Epidemiology of Obesity study. Plasma metabolite profiles were determined using the Biocrates AbsoluteIDQ p150 kit in 176 individuals with normal fasting plasma glucose. VAT was assessed with magnetic resonance imaging and HTGC with proton-MR spectroscopy. We used linear regression to investigate the associations of 190 metabolite variables with VAT and HTGC.ResultsAfter adjustment for age, sex, total body fat, currently used approximations of visceral and liver fat, and multiple testing, three metabolite ratios were associated with VAT. The strongest association was the lysophosphatidylcholines to total phosphatidylcholines (PCs) ratio [- 14.1 (95% CI - 21.7; - 6.6) cm2 VAT per SD of metabolite concentration]. Four individual metabolites were associated with HTGC, especially the diacyl PCs of which C32:1 was the strongest at a 1.31 (95% CI 1.14; 1.51) fold increased HTGC per SD of metabolite concentration.ConclusionMetabolomics may be a useful tool to identify biomarkers of visceral fat and liver fat content that have added diagnostic value over current approximations. Replication studies are required to validate the diagnostic value of these metabolites.
| S-EPMC6778586 | biostudies-literature