International Journal of Obesity最新文献

The worldwide health emergency of obesity is closely connected to how dietary fats are metabolized, whereas the process is significantly influenced by pancreatic lipase (PL), an enzyme critical for lipid hydrolysis into fatty acids. This narrative review employs a methodological approach utilizing literature searches of PubMed data up to March 2024. The search term criteria encompasses keywords related to the role, mechanism, challenges, and current and future treatments of pancreatic lipase in obesity with an overall references is 106. This paper offers a comprehensive explanation of the role of PL, underlining its significance in the digestive process and lipid imbalances that contribute to obesity and by extension, its impact on obesity development and progression. Additionally, it delves into the dual functionality of the pancreas, emphasizing its impact on metabolism and energy utilization which, when dysregulated, promotes obesity. A focal point of this review is the investigation into the efficacy, challenges, and adverse effects of current pancreatic lipase inhibitors, with orlistat being highlighted as a primary current drug delivery. By discussing advanced obesity treatments, including the exploration of novel anti-obesity medications that target specific biological pathways, this review underscores the complexity of obesity treatment and the necessity for a multifaceted approach. In conclusion, this paper emphasizing the importance of understanding the role of enzymes like pancreatic lipase mechanistic and adopting a multidisciplinary approach to treatment and side effects of current obesity drugs and explore new emerging therapeutic strategies for more effective obesity management.

Background: Body composition influences physical fitness (PF) and risk of musculoskeletal injury (MSKI). Assessing the relationship between body fat (BF), PF and MSKI risk in a large diverse military population may provide evidence basis informing health-care policies, practices, and programs for military and civilian populations.

Objective: Evaluate the validity of expedient methods to estimate BF (e.g., circumference-based equation (CBE) and bioelectrical impedance analysis (BIA)) and investigate relationships between BF and PF with MSKI risk in a large diverse population.

Methods: Participants were 1904 active-duty Soldiers (643 F) representing Army demographics sex, race/ethnicity (R/E), and age. PF, defined as the most recent Army Combat Fitness Test (ACFT) score and incidence of MSKI, were obtained from Army records. BF was determined by dual-energy x-ray absorptiometry (%BF_DXA), bioelectrical impedance analysis (%BF_BIA), and CBE using 3-site (Hodgdon, %BF_HE) and 1-site (Taylor-McClung, %BF_TM) equations. Results were stratified by race and sex, to evaluate differences in accuracy of estimated %BF (weighted root mean squared error from %BF_DXA). Associations of BF and PF with MSKI risk were evaluated with logistic regression.

Results: CBE and BIA underestimated %BF compared to %BF_DXA. %BF_BIA differed from %BF_DXA overall and by sex. %BF_TM underestimation was uniform across both sex and R/E compared to %BF_DXA. Mean differences from %BF_DXA by sex (M;F) were lower when measured by %BF_TM (4.38; 4.59) compared to %BF_HE (5.88; 4.39). Individuals had a greater likelihood of MSKI if they failed BF standards (odds ratio 1.32). Scoring ≥ 540 total on ACFT exhibited a 31% (95% CI: 0.52, 0.92) lower MSKI risk during the following 12 months than those with a lower score.

Conclusions: A single-site BF equation (%BF_TM) maintained similar accuracy across the Soldier population by sex, age, and R/E. Implementing a PF score threshold in lieu of passing Army BF standards was associated with lower MSKI risk.

Background: Obesity is related with increased risk for carpal tunnel syndrome (CTS). The effect of bariatric surgery (BS) on the incidence of nerve entrapments is undetermined. We aimed to evaluate the incidence of CTS following BS in a large cohort study.

Methods: A retrospective cohort study of patients with obesity who underwent BS was conducted. The incidence of CTS in the 5-years pre- and post BS was compared. Patients who developed CTS following BS were compared to those who did not.

Results: Six-thousand, one-hundred and twenty-four patients met the inclusion criteria. The average age was 41.2 (SD 12.9) years, most were female (68.6%). The average pre-operative BMI was 42.9 (SD 5.4). Most patients underwent restrictive surgery. The incidence of CTS at the 5-years prior to the BS was significantly higher than the post BS incidence, 8.4% versus 5.1% respectively (p < 0.001) despite the aging of the cohort. Patients who developed CTS following the BS were older and had a higher prevalence of hypertension and diabetes mellitus prior to the BS. They had a higher BMI and excess body weight at every time point measured and a lower BMI reduction. Weight regain was not associated with increased incidence of CTS. Finally, a direct correlation between excess weight loss to greater reduction in the incidence of CTS was noted.

Conclusions: BS was found to be associated with reduced incidence of developing CTS. There is a dose-response association where greater weight loss following BS is protective of developing CTS.

Objective: Obesity in pregnancy increases risk of preterm birth (PTB), a leading cause of infant mortality and morbidity. The heritability of obesity suggests associations of grandmaternal obesity with grandoffspring outcomes, but a potential effect on PTB has not been interrogated. We studied whether grandmaternal (F0 generation) body mass index (BMI) in early pregnancy was related to grandoffspring (F2 generation) PTB risk by type, and to maternal (F1 generation) preeclampsia risk.

Methods: Among 315,240 singleton live-born infants from a countrywide three-generation Swedish cohort, we compared risks of spontaneous and medically indicated PTB, defined as gestational age <37 completed gestation weeks, between categories of maternal grandmaternal BMI in early pregnancy. We also interrogated associations of grandmaternal BMI categories with risk of maternal preeclampsia, a major cause of medically indicated PTB. We assessed whether the associations were mediated through consequences of obesity. In a subset, we examined associations with paternal grandmaternal BMI. To address unmeasured confounding by shared familial factors, we assessed the associations of parental full sisters' BMI with PTB.

Results: Maternal grandmaternal obesity (BMI ≥ 30.0) was related to increased risks of grandoffspring medically indicated PTB and maternal preeclampsia, compared with normal BMI. Adjusted hazard and risk ratios (95% confidence intervals) were, respectively, 1.54 (1.28, 1.86) and 1.32 (1.16, 1.49). Maternal sisters' BMI was unrelated to PTB or preeclampsia risks. Maternal obesity or preeclampsia mediated most (85%) of the maternal grandmaternal obesity-grandoffspring medically indicated PTB association, whereas the association with maternal preeclampsia was primarily mediated (61%) through maternal obesity. There were no associations with spontaneous PTB. Paternal grandmaternal obesity was unrelated to grandoffspring's PTB risk.

Conclusion: Medically indicated PTB in grandoffspring is associated with maternal grandmaternal obesity.

Background: Maternal pre-pregnancy obesity may negatively affect offspring outcomes, including neurodevelopment. This study examined the relationship between maternal pre-pregnancy body mass index (MBMI) and the microstructure of the hippocampus and amygdala in neonates.

Methods: Diffusion tensor imaging was used to assess mean diffusivity (MD) in these brain regions in 122 infants (mean gestational age: 39.9 weeks, mean age at scan: 24.8 days) from the FinnBrain Birth Cohort Study ( www.finnbrain.fi ). Linear regression was applied to explore associations between MBMI and MD at the regional level, while non-parametric permutation analysis was used for voxelwise investigations.

Results: A positive association was found between MBMI and hippocampal MD, particularly in the right hippocampus. Voxelwise analyses showed stronger associations in distinct areas: posterior for the right hippocampus and anterior for the left. No significant association was found between MBMI and amygdala MD.

Conclusion: These findings suggest that in utero exposure to high MBMI may influence hippocampal microstructure in infants, underscoring the need for further research on the intergenerational effects of maternal obesity on early brain development.

Objectives: Altered appetite-related gut hormone concentrations may reflect a physiological adaptation facilitating weight regain after weight loss. This review investigates hormonal changes after weight loss achieved through calorie restriction (CR), exercise (EX), or both combined (CREX).

Methods: A systematic search of PubMed (MEDLINE), EMBASE, SPORTDiscus, Cochrane Library, Web of Science, and ClinicalTrials.gov was conducted to identify randomised controlled trials (RCTs) and non-RCTs reporting in a fasting state either pre- and post-intervention appetite-related hormone concentrations or the changes therein after weight loss. The hormones examined were ghrelin, peptide tyrosine tyrosine (PYY), glucagon-like peptide -1 (GLP-1), and cholecystokinin (CCK), in their total and/or active form. Standardised mean differences (SMD) were extracted as the effect size.

Results: 127 studies were identified: 19 RCTs, 108 non-RCTs, 1305 and 4725 participants, respectively. In response to weight loss induced by CR, EX or CREX, the meta-analysis revealed an increase in total ghrelin from both RCTs (SMD: 0.55, 95% CI: 0.07-1.04) and non-RCTs (SMD: 0.24, 95% CI: 0.14-0.35). A decrease in acylated ghrelin was identified for RCTs (SMD: -0.58, 95% CI: -1.09 to -0.06) but an increase was observed for non-RCTs (SMD: 0.15, 95% CI: 0.03 to 0.27). Findings also revealed a decrease in PYY (total PYY: SMD: -0.17, 95%CI: -0.28 to -0.06; PYY_3-36: SMD: -0.17, 95%CI: -0.32 to -0.02) and active GLP-1 (SMD: -0.16, 95% CI: -0.28 to -0.05) from non-RCTs. Changes in hormones did not differ among the three interventions when controlling for weight loss. Meta-regression indicated that greater weight loss was associated with a greater increase in total ghrelin.

Conclusions: Weight loss induced by CR, EX, or CREX elicits an increase in total ghrelin, but varied responses in other appetite-related hormones. The extent of weight loss influences changes in appetite-related gut hormone concentrations.

Background/objective: Obesity is a devastating worldwide metabolic disease, with the highest prevalence in children and adolescents. Obesity impacts neuronal function but the fate of functional hyperemia, a vital mechanism making possible cerebral blood supply to active brain areas, is unknown in organisms fed a high-caloric Western Diet (WD) since adolescence.

Subjects/methods: We mapped changes in cerebral blood volume (CBV) in the somatosensory cortex in response to whisker stimulation in adolescent, adult, and middle-aged mice fed a WD since adolescence. To this aim, we used non-invasive and high-resolution functional ultrasound imaging (fUS).

Results: We efficiently mimicked the metabolic syndrome of adolescents in young mice with early weight gain, dysfunctional glucose homeostasis, and insulinemia. Functional hyperemia is compromised as early as 3 weeks of WD and remains impaired after that in adolescent mice. These findings highlight the cerebrovascular vulnerability to WD during adolescence. In WD, ω-6:ω-3 polyunsaturated fatty acids (PUFAs) ratio is unbalanced towards proinflammatory ω-6. A balanced ω-6:ω-3 PUFAs ratio in WD achieved by docosahexaenoic acid supplementation efficiently restores glucose homeostasis and functional hyperemia in adults.

Conclusions: WD triggers a rapid impairment in cerebrovascular activity in adolescence, which is maintained at older ages, and can be rescued by a PUFA-based nutraceutical approach.

Objective: Obesity is known to be associated with inflammation and impaired sleep quality. In addition, the anti-inflammatory properties of the daily diet provide positive effects on health. The aim of this study was to investigate the relationship between the inflammatory index of the diet consumed by people with obesity and inflammatory biomarkers and sleep quality.

Method: This study included 124 people with obesity (F: 75; M: 49) with a mean age of 42.20 ± 11.00 years, who presented to a dietary outpatient clinic in Malatya between November 2021 and May 2022. Three-day dietary intake records were collected to calculate Dietary Inflammatory Index (DII) scores, which were then compared with inflammatory biomarkers, anthropometric measurements, and sleep quality measures.

Results: Among the biochemical parameters, C-reactive protein (CRP) was found to be significantly higher in the groups with higher DII score (p = 0.006), and CRP (r = 0.258; p = 0.004) and total cholesterol (r = -0.243; p = 0.007) increased significantly with increasing inflammatory score of the diet. As the inflammatory burden of the diet consumed by the participants increased, their Body Mass Index (BMI) also increased (p = 0.009). No significant correlation was found between DII and sleep quality (p = 0.348).

Conclusion: These findings suggest that an anti-inflammatory diet can effectively reduce inflammation and BMI in people with obesity, but has a limited effect on sleep quality. Therefore, it is recommended that dietitians integrate anti-inflammatory dietary strategies for people with obesity into their clinical practice.