bluuebunny/crossref_metadata_2025_split huggingface dataset:
Greater Adherence to Treatment After Bariatric Surgery by the Implementation of a Standardized Protocol for Delivering Care
Authors: Maraschin Clara K , Blume Carina A , Telo Gabriela H , Schaan Beatriz D 
Published: May 2021

Abstract
Bariatric surgery reference centers adopt different protocols of postoperative care including vitamins and minerals supplementation, since there is no consensus in the literature supporting the best approach. We sought to assess the impact of implementing a standardized postoperative care protocol on the adherence to a multidisciplinary team follow-up and the use of vitamin and mineral supplementation for one year after bariatric surgery in a tertiary care public hospital. This study compared a retrospective cohort of patients [n=70; usual care (UC)] who had undergone Roux-en-Y gastric bypass (RYGB) between April 2017 and April 2018 with a prospective cohort of patients [n=64; standardized postoperative protocol (SPP)] who had undergone RYGB between May 2018 and May 2019. The protocol included (1) a pre-scheduled calendar for one-year appointments with surgeons, nutritionists, and endocrinologists, (2) a systematic follow-up trough phone calls by a trained nurse, (3) a standardized vitamins/minerals supplementation during one year, and (4) pre-scheduled laboratory assessment. The initial approach started in the day after the surgery, when the nurse explained post-operative procedures and delivered printed material with the information and schedules. Patients received a standard supplementation free of charge (daily multivitamins with minerals, calcium carbonate 1,500 mg/day, vitramin D 20,000 IU/week, and 5,000 µg of intramuscular vitamin B12 if serum levels were lower than 400 pg/mL). This study was approved by the local Ethics Committee (2018-0183). Among the 134 patients, 86.7% were women, 42.4 ± 10.1 years-old, with preoperative body mass index of 48.5 ± 8.2 kg/m². Adherence to the postoperative care (multidisciplinary team follow-up and laboratory analyses) was 96.9% in the SPP and 81.7% in the UC (p = .003). The SPP attended a greater number of appointments (11 ± 2 vs. 7 ± 2, p &lt;.001), showed a lower prevalence of suboptimal vitamin B12 at 3 months (18.7% vs. 39.5%, p = .03), and had a higher serum vitamin D levels at 3, 6, and 12 months (p &lt;.001). Prevalence of vitamin D deficiency (lower than 20 ng/mL) one year after surgery was 1.6% vs. 24.3% (p &lt;.001) in the SPP and UC, respectively. Only 18.3%, 26.8% and 41% of patients were using vitamin D supplements in the UC after 3, 6 and 12 months, respectively. We conclude that the proposed standardized protocol led to a greater adherence to the postoperative bariatric surgery care, adding attendance to appointments and reducing the incidence of vitamin deficiencies. Further cost-effectivity analysis may be needed to evaluate properly the implementation feasibility of the protocol in other centers. Financial support: CNPq, CAPES, FIPE (HCPA)
Impact of Morbid Obesity on Patients With Hypertriglyceridemia Induced Acute Pancreatitis
Authors: Pudasaini Garima , Shaka Hafeez , Ikechukwu Achebe , Asotibe Jennifer Chiagoziem , Tejeda Emmanuel Palomera , Warraich Muhammad Sheharyar , Rashad Essam 
Published: May 2021

Abstract
Introduction: Obesity is reportedly associated with worse outcome in patients with acute pancreatitis (AP). However, AP has varying etiologies. Hypertriglyceridemia induced acute pancreatitis (HTGP) has sociodemographic variations compared to AP from biliary stones or alcohol. This study aimed to determine the impact of obesity on outcomes of patients with HTGP. Methods: This was a retrospective cohort study of the combined Nationwide Inpatient Sample database for 2016 and 2017. Hospital discharges of patients 18 years and over with HTGP were included. This cohort was divided based on presence of comorbid obesity into three groups- patients without obesity, mild-moderate obesity (MMO) (BMI: 30.0 - 39.9) and morbid obesity (MO) (BMI &gt;=40.0). Primary outcome was inpatient mortality. Secondary outcomes included length of hospital stay (LOS), total hospital charges (THC), discharge diagnoses of hypocalcemia, sepsis, septic shock, acute renal failure (AKI) and acute respiratory failure (ARF). Multivariate regression analysis was used to adjust for patients’ sociodemographic factors, Charlson comorbidity index as well as hospital characteristics as confounders. Results: A total of 104,465 hospitalizations were principally for HTGP, accounting for 18.2% of patients with acute pancreatitis during the study period. Of the patients with HTGP, 13.7% and 10.9% of these patients classified as having MMO and MO respectively. Patients with obesity were significantly younger than patients without obesity.
In patients with MO, there was higher odds of mortality (aOR=1.83, 95% CI: 1.090 – 3.083, p=0.022), while there was no difference in mortality in patients with MMO (aOR 1.09 95% CI: 0.609 – 1.940, p=0.777), both compared with patients without obesity. Patients with MO had increased mean LOS of 0.5 days (95% CI: 0.3 – 0.7, p&lt;0.001) as well as increased THC of $3977 (95% CI: 1467 – 6487, p=0.002) compared to those without obesity. There was no difference in mortality, THC and LOS in patients with MMO. Morbidly obese patients also had increased odds of septic shock (aOR=2.27, 95% CI: 1.297 – 3.972, p=0.007), AKI (aOR=1.28, 95% CI: 1.120 – 1.459, p&lt;0.001), and ARF (aOR=1.94, 95% CI: 1.491 – 2.524, p&lt;0.001). Conclusion: Morbid obesity is associated with higher mortality and poor outcomes in patient with hypertriglyceridemia induced pancreatitis.
Insulin Resistance Shows Stronger Correlation With Ectopic Liver Fat Instead of Visceral Fat in Asian Indians
Authors: Garg Umesh Kumar , Mathur Sandeep Kumar , Mathur Nitish , Purwar Naincy , Kumar Anshul , Tiwari Pradeep , Saxena Aditya 
Published: May 2021

Abstract
Introduction: Insulin resistance (IR) is associated with abdominal obesity. Asian Indians have higher insulin resistance at lower abdominal obesity levels as compared to the western population. However, the relative association of various compartments of abdominal fat, i.e., Subcutaneous Fat (SCAT), Visceral fat (VAT), and ectopic Liver Fat, is not very clear. Our study’s objective was to look for the association of abdominal fat composition in Asian Indians with IR level and gender and diabetes status. Methodology: Our study is an analytical cross-sectional study conducted from 2018–2020 at SMS Hospital located in northwest India. 91 subjects were studied during the study period and underwent MRI for SCAT, VAT, and Liver fat estimation. We divided subjects into tertile groups, based on HOMA-IR levels, and statistical analysis for SCAT, VAT, and Lipid fat in each tertile and as a whole group carried out. Similarly, we analysed data in male and female and diabetic and non-diabetic groups, as tertiles and as a whole. Results: Of the recruited subjects 49 were diabetics (M: F=23:26) and 42 were non-diabetic (M: F=12:30). In the overall group, HOMA-IR has a weak positive association with VAT and Liver Fat and a weak negative association with SCAT (R=0.28,0.38 and -0.11, respectively). From tertile1 to tertile3, there was a consistent increase in VAT and Liver fat (119.3, 121.1, 156.6 cm2 and 8.18, 10.02, 10.89% respectively), so that R value increases from -0.24 to 0.21 for VAT and -0.195 to 0.58 for Liver Fat. On the other hand, the SCAT levels were not different and correlation with IR declined from -0.299 to -0.39. On Sex wise analysis negative correlation of SCAT with IR become substantial from tertile1 to tertile3 in both males and females but strong correlation was seen in females (-0.189 to -0.515) though amount of SCAT was not different among tertiles. Both VAT and Liver Fat increased with tertile1 to terrtile3; IR was very strongly correlated with Liver Fat in both the sexes at higher tertiles (0.91 for males and 0.71 for females). In the diabetic group, liver fat was significantly associated with IR at higher tertile (R=0.9). The SCAT was negatively associated with IR, and a further decline in correlation coefficient with each tertile, became significant at 3rd tertile (-0.41) with a weak correlation of IR with VAT. These relations have similar SCAT and Liver fat trends but a strong correlation not seen in the non-diabetic group. Conclusion: Insulin resistance strongly correlated with ectopic liver fat in Asian Indians including diabetics with no gender disparity which became significant at higher tertile. As compared to ectopic liver fat, VAT has only a minor role in development of IR. SCAT has a protective role against IR in both diabetics and non-diabetics.
Severe Hyperlipidemia With LDL Cholesterol of 393 Milligrams per Decilitre After 7 Months of High Fat Ketogenic Diet: A Rare Case Report
Authors: Swaid Bakr 
Published: May 2021

Abstract
Introduction: Ketogenic diet (KD) is now a popular weight-loss diet with other proclaimed health benefits. KD is largely safe in the short-term especially if done under medical supervision to monitor for well-described side effects like hyperlipidemia among others. We report a case of KD-induced drastic elevation in LDL cholesterol.
Clinical Case: An otherwise healthy 41-year-old male with obesity and a BMI of 35.8 kg/m2 followed KD to help with weight loss. His lipid panel 18 months prior to initiation of KD showed total cholesterol (TC) 171 mg/dL (reference &lt;200 preferred), HDL cholesterol (HDL-C) 49 mg/dL (reference &gt;60 preferred), LDL cholesterol (LDL-C) 99 mg/dL (reference &lt;100 optimal), and a triglyceride (TG) 145 mg/dL (reference &lt;200). During his KD journey, he lost 40 pounds and his BMI became 29.5 kg/m2 after seven months. While on KD, he reported more mental clarity, improved sleep quality, higher energy level, and complete resolution of chronic cystic acne. Seven months after starting KD, his lipid panel showed TC 488.7 mg/dL, HDL-C 54.4 mg/dL, LDL-C 393 mg/dL, VLDL-C 41.5 mg/dL, and triglyceride 207.5 mg/dL. Lipid panel was repeated in 2 days to exclude a possible laboratory error but it confirmed the previous result and repeat LDL-C was 380 mg/dL. Fasting plasma glucose (FPG) was 91 mg/dL. HbA1c was normal at 5.0%. Uric acid was elevated at 8.9 mg/dL (reference 3.4–7.0). High sensitivity C-reactive protein was not elevated at 0.13 mg/dL (reference &lt;0.5). Total 25 hydroxy-vitamin D level was normal at 43.9 ng/mL (reference 30–100). CBC, renal function, and liver function tests were all normal. Since the patient declined statin therapy, he was counseled to decrease saturated fat (e.g. animal-based) intake and to liberalize his carbohydrate intake (i.e. 30% of total calorie intake instead of his baseline of 5–10%). Two weeks after doing so, lipid panel was remarkable for TC 371.2 mg/dL, HDL-C 49.7 mg/dL, LDL-C 279.0 mg/dL, VLDL-C 42.26 mg/dL and TG 211.3 mg/dL. Six weeks from the initial lipid panel, repeat testing showed TC 266.2 mg/dL, HDL-C 54.4 mg/dL, LDL-C 190.0 mg/dL, VLDL-C 21.64 mg/dL and TG 108.2 mg/dL. The patient remained without any major symptoms, namely no symptoms of cardiovascular disease.
Conclusion: To the best of our knowledge, our patient had the highest reported KD-induced increase in LDL-C (297% increase) despite normal baseline and no history of familial hypercholesterolemia. Dietary modification alone resulted in 29% decrease in 2 weeks and 52% decrease in six weeks. A limitation to this case report is the lack of lipid panel subfractionation as previous studies showed KD to result in a decrease in small LDL particles (atherogenic) and an increase in large LDL particles (non-atherogenic). More research is needed on the long-term health consequences of KD. Despite guidelines on how to manage KD-induced hyperlipidemia are greatly needed, they are lacking.
Untangling the Heterogeneity of Acquired Generalized Lipodystrophy
Authors: Cavdar Umit , Akinci Baris , Foss de Freitas Maria Cristina , Conjeevaram Hari , Fox David , Fontana Robert , Tayeh Marwan , Frame David , Innis Jeffrey , Walkovich Kelly , Oral Elif A 
Published: May 2021

Abstract
Acquired generalized lipodystrophy (AGL) is characterized by extensive adipose tissue loss, subsequent development of metabolic disease with severe insulin resistance and hypertriglyceridemia and a varying spectrum of autoimmune or immune-dysregulatory features. We recently evaluated twelve patients (8 females, 4 males; age range: 14 - 54 years). The reported onset of fat loss varies from age 2 to 31 years of age but most patients presenting between age 3 and 19 years. The age of diagnosis varies from 4 to 53 years. Clinical panniculitis was reported in 4 patients. Although adipose tissue loss occurred in a generalized fashion, several patients had measured body fat as high as 35 percent on DEXA scans with leptinemia also covering a spectrum from undetectable levels to as high as 6.2 ng/ml. All patients had insulin resistance. Eight patients had diabetes (4 had type 1 diabetes). Dyslipidemia was diagnosed in 11 patients. Hepatic steatosis and/or elevated liver function tests were detected in all subjects. The liver disease was varied and had distinctive characteristics of episodic increases in liver tests in 4 with development of portal hypertension and splenomegaly. These patients had periportal lymphocytic and eosinophilic infiltration on liver biopsies when undertaken during transaminitis and developed portal hypertension, splenomegaly and biliary obstruction while preserving synthetic liver function over time, suggesting that their clinical course may be consistent with nodular regenerative hyperplasia (NRH). Patients also developed a wide range of immune-dysregulatory features including IgA deficiency, common variable immunodeficiency, autoimmune hives, angioedema, eczematous dermatitis, autoimmune hypothyroidism, Graves’ disease, atrophic gastritis, juvenile dermatomyositis, rheumatoid arthritis, polyarthritis, immune thrombocytopenia, cutaneous morphea, lentigo, peripheral T cell lymphoma, graft versus host disease, hemophagocytic syndrome, interstitial lung disease, autoimmune hemolytic anemia, autoimmune colitis, Crohn disease, and periodic fevers. Low complement 4 levels were detected in 5 patients, and 3 had low complement 3 levels. Genetic workup revealed CTLA-4 haploinsufﬁciency in one case and variants of uncertain significance in P4HA3, TTN, TNFRSF13B, and NLRP3 genes in several others. One distinctive patient was heterozygous for a pathogenic LRBA variant. The exact etiology of AGL is unknown and heterogeneity creates a diagnostic challenge. While panniculitis is a distinct initial presentation in some cases, immune dysregulation affecting multiple organs with accompanying NRH may constitute a new subgroup of AGL. Immune check-point perturbation via gremlin mutation may also lead to AGL. Collective review of cases with predetermined clinical and laboratory evaluation criteria may be helpful to describe subgroups of AGL.
Adipocyte-Derived Lactate Potentiates Obesity-Evoked Adipose Macrophage Inflammation
Authors: Hui Xiaoyan Hannah , Feng Tianshi 
Published: May 2021

Abstract
Introduction: Obesity is characterized by mobilization of macrophage inflammation, which represents the major events of obesity-associated adipose tissue inflammation. . On the other hand, lactate accumulation in adipose tissue long been observed. However, whether elevation of lactate plays an essential role in adipose inflammation is not known. In this study, we sought to examine the intermediary role of lactate in macrophage polarization and adipose inflammation upon obesity. Method: Lactate level and activity of lactate dehydrogense (LDH), the key enzyme of lactate production, were measured by biochemical assays. Adipocyte- and macrophage- specific Ldha knock out mice were constructed by cre-LoxP system to study the physiological role of lactate in diet induced obesity. Macrophage polarization and inflammation were examined by western blotting and Q-PCR. Results: Lactate and LDH activity were selectively upregulated in adipose tissues of obese mice. Adipocyte-, but not macrophage-selective deletion of LDHA, led to a significant improvement of adipose inflammation and metabolic dysfunctions. In vitro experiments showed that the lactate promoted M1 polarization through direct interation and inhibition of the PHD2, which subsequently stabilizes HIF-1alpha. In addition, a positive correlation between adipose lactate level and adipose tissue inflammation was found in obese patients. Conclusion: In obese condition, increased production of lactate from adipocytes enhances adipose tissue inflammation by promoting the proinflammatory polarization of adipose macrophages.
Fatty Acids Modify the MicroRNA Content of Exosomes Released by Hypothalamic Astrocytes and the Response of POMC Neurons to These Exosomes
Authors: Collado-Pérez Roberto , García-Piqueres Jorge , Jiménez-Hernaiz María , Argente Jesús , Belsham Denise D , Frago Laura M , Chowen Julie A 
Published: May 2021

Abstract
It is now clear that hypothalamic astrocytes participate in maintaining metabolic homeostasis. Both nutrients and metabolic hormones can directly impact on these glial cells to modify their release of gliotransmitters, metabolic factors, growth factors, etc, as well as their physical interaction with neighboring neurons. Another mechanism by which astrocytes could communicate with neurons is through their release of exosomes. We have previously shown (by RNAseq analysis) that exposure to palmitic acid (PA) dramatically modifies the miRNA content of exosomes released by hypothalamic astrocytes. Here our objectives were: 1) To determine if the miRNA changes in hypothalamic astrocyte-derived exosomes in response to oleic acid (OA) differ from those seen in response to PA and 2) Analyze the response of POMC neurons to exosomes derived from astrocytes exposed to either PA or OA. Primary hypothalamic astrocyte cultures were treated with PA (0.5 mM), OA (0.5 mM) or vehicle (V) for 24 hours. Exosomes were purified from the media and used for miRNA analysis and to treat a POMC neuronal cell line (mHypoA-POMC/GFP-1). Both OA and PA modified miRNA levels in exosomes compared to those detected in V exosomes, but these modifications differed between the two fatty acids. Furthermore, the response of POMC neurons to exosomes from vehicle (E-V), OA (E-OA) and PA (E-PA) treated astrocytes for 24 hours differed significantly. The expression of POMC mRNA was significantly decreased in response to E-V and increased in response to both E-OA and E-PA, although the increase in POMC mRNA was significantly greater in E-PA treated neurons. These results suggest that hypothalamic astrocytes can directly communicate with neurons involved in metabolic control through exosomes and that the messages contained within these exosomes are modulated by the nutrient environment.
Identification of Key Genes and Pathways for Childhood Obesity Using System Biology Approach Based on Comprehensive Gene Information
Authors: Crispim Daisy , Pellenz Felipe Mateus , Assmann Tais Silveira 
Published: May 2021

Abstract
Introduction: Childhood obesity is one of the most important public health issues of the 21st century. Epidemiological studies have suggested that obesity during childhood increases the risk of developing comorbidities, such as type 2 diabetes, later in life. Childhood obesity is a complex disease whose molecular mechanisms are not completely elucidated. In this context, a system biology approach could contribute to the scientific knowledge regarding genetic factors related to childhood obesity onset. Aim: To identify molecular mechanisms involved in childhood obesity by implementing a system biology approach. Methods: Experimentally validated and computationally predicted genes related to Pediatric Obesity (C2362324) were downloaded from the DisGeNET v7.0 database. The protein-protein interaction (PPI) network was constructed using the STRING v11.0 database and analyzed using NetworkAnalyst v3.0 and Cytoscape v3.8.1. The relevance of each node for the network structure and functionality was assessed using the degree method to define hub genes. Functional and pathway enrichment analyses were performed based on Gene Ontology (GO) terms and KEGG Pathways. Results: The search on the DisGeNET database retrieved 191 childhood obesity-related genes. The PPI network of these genes showed 19 hub genes (STAT3, SIRT1, BCL2, IRS1, PPARG, SOCS3, TGFB1, HDAC4, DNMT1, ADCY3, PPARA, NEDD4L, ACACB, NR0B2, VEGFA, APOA1, GHR, CALR, and MKKS). These hub genes were involved in biological processes of lipid storage / kinase activity, regulation of fatty-acid metabolic processes, regulation of pri-miRNA transcription by RNA polymerase II, and negative regulation of small molecules and carbohydrate metabolic processes. In terms of molecular functions, repressing of transcription factors biding was found enriched. Regarding KEGG Pathways, the hub genes are involved with adipocytokine signaling, insulin resistance, longevity regulation, and cytokine signaling pathways. Conclusion: Our approach identified 19 hub genes, which are highly connected and probably have a key role in childhood obesity. Moreover, functional enrichment analyses demonstrated they are enriched in several biological processes and pathways related to the underlying molecular mechanisms of obesity. These findings provide a more comprehensive information regarding genetic and molecular factors behind childhood obesity pathogenesis. Further experimental investigation of our findings may shed light on the pathophysiology of this disease and contribute to the identification of new therapeutic targets.