Manngrau9376
Diets high in fat and sugar induce inflammation throughout the body, particularly along the gut-brain axis; however, the way these changes in immune signaling mediate one another remains unknown. We investigated cytokine changes in the brain and colon following prolonged high fat or sugar diet in female and male adult C57BL/6 mice. Ten weeks of high fat diet increased levels of TNFα, IL-1β, IL-6, IFNγ, and IL-10 in the female hippocampus and altered cytokines in the frontal cortex of both sexes. High sugar diet increased hippocampal cytokines and decreased cytokines in the diencephalon and frontal cortex. In the colon, high fat diet changed cytokine expression in both sexes, while high sugar diet only increased TNFα in males. Rapamune Causal mediation analysis confirmed that colon IL-10 and IL-6 mediate high fat diet-induced neuroimmune changes in the female hippocampus and male frontal cortex. Additionally, high fat diet increased food consumption and weight gain in both sexes, while high sugar diet decreased male weight gain. These findings reveal a novel causal link between gut and brain inflammation specific to prolonged consumption of high fat, not high sugar, diet. Importantly, this work includes females which have been under-represented in diet research, and demonstrates that diet-induced neuroinflammation varies by brain region between sexes. Furthermore, our data suggest female brains are more vulnerable than males to inflammatory changes following excessive fat and sugar consumption, which may help explain the increased risk of inflammation-associated psychiatric conditions in women who eat a Western Diet rich in both dietary components.The adipocytes play an important role in driving the obese-state-white adipose tissue (WAT) stores the excess energy as fat, wherein brown adipose tissue (BAT) is responsible for energy expenditure via the thermoregulatory function of uncoupling protein 1 (UCP1)-the imbalance between these two onsets obesity. Moreover, the anti-obesity effects of brown-like-adipocytes (beige) in WAT are well documented. Browning, the process of transformation of energy-storing into energy-dissipating adipocytes, is a potential preventive strategy against obesity and its related diseases. In the present study, to explore an alternative source of natural products in the regulation of adipocyte transformation, we assessed the potential of theobromine (TB), a bitter alkaloid of the cacao plant, inducing browning in mice (in vivo) and primary adipocytes (in vitro). Dietary supplementation of TB significantly increased skin temperature of the inguinal region in mice and induced the expression of UCP1 protein. It also increased the expression levels of mitochondrial marker proteins in subcutaneous adipose tissues but not in visceral adipose tissues. The microarray analysis showed that TB supplementation upregulated multiple thermogenic and beige adipocyte marker genes in subcutaneous adipose tissue. Furthermore, in mouse-derived primary adipocytes, TB upregulated the expression of the UCP1 protein and mitochondrial mass in a PPARγ ligand-dependent manner. It also increased the phosphorylation levels of PPARγ coactivator 1α without affecting its protein expression. These results indicate that dietary supplementation of TB induces browning in subcutaneous WAT and enhances PPARγ-induced UCP1 expression in vitro, suggesting its potential to treat obesity.A diet high in saturated fat leads to skeletal muscle deteriorations including insulin resistance, mitochondrial dysfunction and muscle fiber atrophy. Consumption of long-chain polyunsaturated fatty acids and exercise have shown promise in ameliorating high-fat diet (HFD)-induced oxidative stress and inflammation. However, the impact of extra virgin olive oil (EVOO) on mitochondrial homeostasis in muscle is largely unknown. This study aimed to investigate whether 12 weeks of EVOO feeding alone and in conjunction with endurance training could protect against metabolic and mitochondrial dysfunction rat muscle with HFD. Female Sprague-Dawley rats were divided into 4 groups fed a control diet (C), HFD, EVOO diet, and EVOO diet with training (EVOO+T). Mitochondrial enzyme activity and protein content decreased with HFD compared to C, but were restored with EVOO and EVOO+T. EVOO+T elevated muscle cytochrome c and PGC-1α levels. HFD increased muscle proteolytic markers and protein ubiquitination, whereas these effects were not seen in EVOO and EVOO+T. HFD suppressed mitochondrial fusion protein level while increasing fission protein levels, but were restored with EVOO and EVOO+T. Mitophagy marker PINK1 content decreased with HFD, but was unchanged in EVOO and EVOO+T. EVOO+T upregulated autophagy markers, along with decreased phosphorylated/dephosphorylated FoxO3 ratio. Antioxidants enzyme levels were upregulated by EVOO and EVOO+T, and EVOO+T reduced HFD-induced lipid peroxidation. In conclusion, HFD impaired muscle oxidative capacity, promoted protein ubiquitination and mitochondrial fission, and upregulated autophagy markers. Replacement of HFD with EVOO corrected the observed adverse effects, while exercise training in conjunction with EVOO provided additional protection to the muscle.Osteoporosis, a disease characterized by low bone density that poses a high risk of bone fractures, is associated with aging, diet, and menopause. Despite the various known therapeutic methods for osteoporosis treatment, the development of a new therapeutic agent without side effects in long-term use is required. Cinnamic acid (CA) is a phytochemical found in cinnamon. In this study, we evaluated the effect of CA on osteoporosis and demonstrated its mechanism in MC3T3E1 preosteoblasts and ovariectomized mice. CA treatment induced osteoblast differentiation with elevation of osteogenic markers both in vitro and in vivo. CA treatment ameliorated bone loss resulting in better bone indices, increased gut microbial diversity, and recovered changes in the gut microbial composition induced by ovariectomy. These changes were accompanied by an increase in BMP/TGFβ/Smad signaling. Therefore, CA has the potential to suppress the progress of bone loss via the enhancement of bone density through the regulation of gut microbiota.Neuroinflammation is a central factor in neuropathic pain (NP). Ginger is a promising bioactive compound in NP management due to its anti-inflammatory property. Emerging evidence suggests that gut microbiome and gut-derived metabolites play a key role in NP. We evaluated the effects of two ginger root extracts rich in gingerols (GEG) and shogaols (SEG) on pain sensitivity, anxiety-like behaviors, circulating cell-free mitochondrial DNA (ccf-mtDNA), gut microbiome composition, and fecal metabolites in rats with NP. Sixteen male rats were divided into four groups sham, spinal nerve ligation (SNL), SNL+0.75%GEG in diet, and SNL+0.75%SEG in diet groups for 30 days. Compared to SNL group, both SNL+GEG and SNL+SEG groups showed a significant reduction in pain- and anxiety-like behaviors, and ccf-mtDNA level. Relative to the SNL group, both SNL+GEG and SNL+SEG groups increased the relative abundance of Lactococcus, Sellimonas, Blautia, Erysipelatoclostridiaceae, and Anaerovoracaceae, but decreased that of Prevotellanger on gut-brain axis in pain management.
The modified Ferriman-Gallwey (mFG) diagram for scoring hirsutism uses images with traditionally Eurocentric feminine features. No reports have documented its utility in patients with other gender identities.
A 16-year-old non-binary masculine patient, sex assigned female at birth, was seen for hyperandrogenism and irregular menses. They declined an exam citing body dysphoria, and declined self-documenting on the mFG diagram, expressing anxiety with gendered images. We subsequently developed a novel, gender-inclusive mFG diagram, which the patient was then comfortable using to document their hair pattern.
This case documents how the binary gendered characteristics of the mFG diagram can impact the care of patients. As gender expression is highly individual, we created the first gender-inclusive version of the mFG diagram to enhance care for all patients.
This case documents how the binary gendered characteristics of the mFG diagram can impact the care of patients. As gender expression is highly individual, we created the first gender-inclusive version of the mFG diagram to enhance care for all patients.
The incidence and risk factors of obstetric perineal tears occurrence in vaginal delivery of adolescent pregnant patients are not well-established. We aimed to describe the incidence of obstetric perineal tears in adolescents and the maternal- obstetric risk factors associated with this situation.
Retrospective cohort study.
Department of Obstetrics and Gynecology, Tepecik Education and Research Hospital, Izmir, Turkey PARTICIPANTS Adolescent pregnant patients (≤ 19 years) who delivered vaginally in our institution between January 2014 and January 2021.
The main outcome measures were the incidence of perineal tears, the degree of perineal tears, and the risk factors associated with severe perineal tears in adolescents. Severe perineal tears include 3rd and 4th degree lacerations. Third-degree tear is defined as partial or complete disruption of the anal sphincter muscles, and fourth-degree tear is defined as lacerations involving the rectal mucosa.
A total of 3441 adolescents who had a vaginal delivery were included in the study. The rate of severe perineal tear was 5.8% (200/3441). Risk factors associated with obstetric laceration in adolescents in multivariate analysis were nulliparity (OR 1.72, 95% CI 1.14-2.41, p=0.007), high birth weight (OR 4.1, 95% CI 2.71-6.21, p<0.001), and labor induction (OR 1.36, 95% CI 1.01-1.85, p=0.02). Spontaneous onset of labor and previous delivery reduced the risk of severe perineal tear in adolescent pregnant patients (respectively; OR 0.68,95% CI 0.51-0.94, p=0.02 and OR 0.51, 95% CI 0.33-0.79, p=0.007).
In adolescents, the risk of severe perineal tear was associated with nulliparity, birth weight, and labor induction. The only possible modifiable risk factor was labor induction.
In adolescents, the risk of severe perineal tear was associated with nulliparity, birth weight, and labor induction. The only possible modifiable risk factor was labor induction.
Evaluate the impact of nitrous oxide on patient reported pain for placement of intrauterine systems (IUSs) in adolescents.
Prospective observational study.
Intrauterine system placement in an ambulatory clinic compared to placement with nitrous oxide in a hospital-based sedation unit.
English-speaking adolescents aged 12 to 20 presenting to a pediatric and adolescent gynecologist with a medical indication for IUS placement.
Patient reported procedural pain measured on a visual analog score (VAS) two minutes post IUS insertion procedure. Secondary outcome measurement of likelihood of recommending an IUS to a peer.
Seventy-four patients agreed to participate. Forty-five patients underwent intrauterine system placement in clinic. Controlling for age, history of dysmenorrhea, and body mass index, a significant time (change in reported pain scores pre- vs. post IUS insertion) by treatment (nitrous oxide versus standard-of-care) interaction was observed for patient reported pain (b = -29.32mm, p < .01).
