Modify Body Weight Research Articles

Nutraceuticals and Herbal Food Supplements for Weight Loss: Is There a Prebiotic Role in the Mechanism of Action?

Numerous nutraceuticals and botanical food supplements are used with the intention of modulating body weight. A recent review examined the main food supplements used in weight loss, dividing them according to the main effects for which they were investigated. The direct or indirect effects exerted on the intestinal microbiota can also contribute to the effectiveness of these substances. The aim of this review is to evaluate whether any prebiotic effects, which could help to explain their efficacy or ineffectiveness, are documented in the recent literature for the main nutraceuticals and herbal food supplements used for weight loss management. Several prebiotic effects have been reported for various nutraceutical substances, which have shown activity on Bifidobacterium spp., Lactobacillus spp., Akkermansia muciniphila, Faecalibacterium prausnitzi, Roseburia spp., and the Firmicutes/Bacteroidetes ratio. Different prebiotics have beneficial effects on weight and the related metabolic profile, in some cases even acting on the microbiota with mechanisms that are completely independent from those nutraceuticals for which certain products are normally used. Further studies are necessary to clarify the different levels at which a nutraceutical substance can exert its action.

Effect of cinnamon on blood sugar and anthropometric measurement in type two diabetes patients

There is some emerging evidence that suggests certain supplements help lower blood sugar levels. One of these is cinnamon, which exhibits characteristics that mimic insulin, such as the activity of biologically active substances to activate insulin receptor kinase, increasing glucose uptake, autophosphorylation of the insulin receptor, and glycogen synthase activity. To assess the effect of the cinnamon substance on lowering fasting blood sugar, modifying body weight, body mass index (B.M.I.), and waist circumference in type two diabetics. A randomized controlled intervention clinical trial. The study was conducted on 60 patients with type II diabetes mellitus; the study followed both gender patients for four weeks. The contributors were allocated randomly into a group that receives 2 g/d cinnamon substance (intervention group), and a group without cinnamon substance is given (control group). Fasting plasma glucose (F.P.G.) and anthropometrics measurement at the beginning (beforehand cinnamon supplementation and 4week at the end of the study duration). After 4 weeks of cinnamon taken, serum F.P.G. levels significantly improved (P≤0.0001). Anthropometric measurements (weight, height, B.M.I.) were reduced significantly (change mean ≤ P=0.001) for all. The Present study disclosed that supplementation of 2 gm cinnamon improves F.P.G. and has a good role in anthropometric indices (weight, waist circumference, B.M.I.).

The Peripheral Cannabinoid Receptor Type 1 (CB1) as a Molecular Target for Modulating Body Weight in Man.

The cannabinoid 1 (CB1) receptor regulates appetite and body weight; however, unwanted central side effects of both agonists (in wasting disorders) or antagonists (in obesity and diabetes) have limited their therapeutic utility. At the peripheral level, CB1 receptor activation impacts the energy balance of mammals in a number of different ways: inhibiting satiety and emesis, increasing food intake, altering adipokine and satiety hormone levels, altering taste sensation, decreasing lipolysis (fat break down), and increasing lipogenesis (fat generation). The CB1 receptor also plays an important role in the gut–brain axis control of appetite and satiety. The combined effect of peripheral CB1 activation is to promote appetite, energy storage, and energy preservation (and the opposite is true for CB1 antagonists). Therefore, the next generation of CB1 receptor medicines (agonists and antagonists, and indirect modulators of the endocannabinoid system) have been peripherally restricted to mitigate these issues, and some of these are already in clinical stage development. These compounds also have demonstrated potential in other conditions such as alcoholic steatohepatitis and diabetic nephropathy (peripherally restricted CB1 antagonists) and pain conditions (peripherally restricted CB1 agonists and FAAH inhibitors). This review will discuss the mechanisms by which peripheral CB1 receptors regulate body weight, and the therapeutic utility of peripherally restricted drugs in the management of body weight and beyond.

Adipose expression of CREB3L3 modulates body weight during obesity

We found the hepatic transcription factor Cyclic-AMP Responsive Element Binding Protein 3-like-3 (CREB3L3) to be expressed in adipose tissue, and selectively downregulated in the more metabolically protective subcutaneous adipose tissue in obese mice and humans. We sought to elucidate the specific role of this factor in adipose biology. CREB3L3 fat-specific knockout mice were fed a high-fat diet to induce obesity and metabolic dysfunction. Additionally, we injected a flip-excision adeno-associated virus directly into the subcutaneous inguinal adipose tissue of Adiponectin-Cre mice to create a depot-specific overexpression model for further assessment. Fat-specific ablation of CREB3L3 enhanced weight gain and insulin resistance following high-fat feeding, as fat-specific knockout mice expended less energy and possessed more inflammatory adipose tissue. Conversely, inguinal fat CREB3L3 overexpression deterred diet-induced obesity and ameliorated metabolic dysfunction. Together, this study highlights the relevance of CREB3L3 in obese adipose tissue and demonstrates its role as a powerful body weight modulator.

898-P: Colonic Acetate Production in Youth with and without Obesity

Recent studies suggest that gut microbiota can modulate body weight via products of bacterial fermentation. We tested the hypothesis that, for the same amount of fermentable carbohydrate, lean and obese youth have a different capability to produce acetate in the colon. We also tested the effect of colonic fermentation on plasma glucose, insulin, C-peptide, and free fatty acids (FFA). 38 youth, ages 15 to 21 yr (19 lean/19 obese) underwent a 10-hour sodium [d3]-acetate intravenous infusion to determine the rate of appearance of acetate (Ra) in plasma before and after 20g of lactulose (per os). Pre- and post- Ra values were determined at a quasi-steady state. Compared to obese youth, lean showed a larger increase in Ra after colonic fermentation (P=0.001). Plasma FFA concentrations declined from 0 to 300 minutes (nadir), with a greater reduction in lean youth (P=0.042). Insulin, glucose, and C-peptide levels were lower at the end of the study than at baseline in both groups (all P 0.05). These data suggest that 1) obese youth either ferment lactulose to a lesser degree or experience a higher hepatic uptake of acetate; 2) acetate may cause a reduction in FFA during the fasting state that is more marked in lean youth; 3) acetate may be associated with changes in glucose metabolism, although herein, it is difficult to differentiate between the effect of acetate infusion and prolonged fasting. Disclosure B. Galuppo: None. G. Cline: None. M. A. Van name: None. C. Agazzi: None. C. L. Kien: None. N. Santoro: None. Funding National Institute of Diabetes and Digestive and Kidney Diseases (R01DK114504)

Combined nicotinamide N-methyltransferase inhibition and reduced-calorie diet normalizes body composition and enhances metabolic benefits in obese mice

Obesity is a large and growing global health problem with few effective therapies. The present study investigated metabolic and physiological benefits of nicotinamide N-methyltransferase inhibitor (NNMTi) treatment combined with a lean diet substitution in diet-induced obese mice. NNMTi treatment combined with lean diet substitution accelerated and improved body weight and fat loss, increased whole-body lean mass to body weight ratio, reduced liver and epididymal white adipose tissue weights, decreased liver adiposity, and improved hepatic steatosis, relative to a lean diet substitution alone. Importantly, combined lean diet and NNMTi treatment normalized body composition and liver adiposity parameters to levels observed in age-matched lean diet control mice. NNMTi treatment produced a unique metabolomic signature in adipose tissue, with predominant increases in ketogenic amino acid abundance and alterations to metabolites linked to energy metabolic pathways. Taken together, NNMTi treatment’s modulation of body weight, adiposity, liver physiology, and the adipose tissue metabolome strongly support it as a promising therapeutic for obesity and obesity-driven comorbidities.

Beneficial effects of atorvastatin on sex-specific cognitive impairment induced by a cerebral microhaemorrhage in mice.

Cerebral microhaemorrhages (CMHs) are associated with cognitive decline in humans. In rodents, CMHs induces cognitive impairment in male mice along with sex-specific cortical and hippocampal changes affecting neural, glial and vascular functions. Statins, have been proposed to prevent cognitive decline. We tested here the action of atorvastatin on CMH-induced cognitive impairment in a murine model of CMH. Using a multimodal approach combining behavioural tests, in vivo imaging, biochemistry and molecular biology, the effects of oral administration of atorvastatin on the sex-specific changes induced by a cortical CMH were studied in male and female mice (C57BL/6J) at 6-week post-induction using a collagenase-induced model. Atorvastatin caused specific effects according to the sex-specific CMH-induced changes. In males, atorvastatin improved the visuospatial memory, induced a local modulation of microglial response and enhanced brain-derived neurotrophic factor (BDNF)-tropomyosin receptor kinase B (trkB) and vascular endothelial growth factor (VEGF) expression in the cortex. In the hippocampus, atorvastatin increased glucose metabolism and modulated astrocytes morphology. In females, atorvastatin did not modulate visuospatial memory despite the increased expression of cortical BDNF and the decrease in the number of hippocampal astrocytes. Atorvastatin also induced a decrease in the expression of cortical oestrogen receptors but did not modify body weight nor serum cholesterol levels in both sexes. Atorvastatin modulated the sex-specific cognitive impairment induced by the CMH with a pathophysiological impact mainly within the cortical area. It could represent a promising candidate for future sex-stratified clinical trials in patients with CMH.

The Role of Central Neurotensin in Regulating Feeding and Body Weight

The small peptide neurotensin (Nts) is implicated in myriad processes including analgesia, thermoregulation, reward, arousal, blood pressure, and modulation of feeding and body weight. Alterations in Nts have recently been described in individuals with obesity or eating disorders, suggesting that disrupted Nts signaling may contribute to body weight disturbance. Curiously, Nts mediates seemingly opposing regulation of body weight via different tissues. Peripherally acting Nts promotes fat absorption and weight gain, whereas central Nts signaling suppresses feeding and weight gain. Thus, because Nts is pleiotropic, a location-based approach must be used to understand its contributions to disordered body weight and whether the Nts system might be leveraged to improve metabolic health. Here we review the role of Nts signaling in the brain to understand the sites, receptors, and mechanisms by which Nts can promote behaviors that modify body weight. New techniques permitting site-specific modulation of Nts and Nts receptor–expressing cells suggest that, even in the brain, not all Nts circuitry exerts the same function. Intriguingly, there may be dedicated brain regions and circuits via which Nts specifically suppresses feeding behavior and weight gain vs other Nts-attributed physiology. Defining the central mechanisms by which Nts signaling modifies body weight may suggest strategies to correct disrupted energy balance, as needed to address overweight, obesity, and eating disorders.

Dapagliflozin Does Not Modulate Atherosclerosis in Mice with Insulin Resistance.

Type 2 diabetes mellitus (T2DM) increases morbimortality in humans via enhanced susceptibility to cardiovascular disease (CVD). Sodium-glucose co-transporter 2 inhibitors (SGLT2i) are drugs designed for T2DM treatment to diminish hyperglycaemia by reducing up to 90% of renal tube glucose reabsorption. Clinical studies also suggest a beneficial action of SGLT2i in heart failure and CVD independent of its hypoglycaemiant effect. In the present study, we explored the effect of SGLT2i dapagliflozin (DAPA) in the metabolism and atherosclerosis in Apoe−/−Irs2+/− mice, which display accelerated atherosclerosis induced by insulin resistance. DAPA treatment of Apoe−/−Irs2+/− mice, which were fed a high-fat, high-cholesterol diet, failed to modify body weight, plasma glucose or lipid. Carbohydrate metabolism characterisation showed no effect of DAPA in the glucose tolerance test (GTT) despite augmented insulin levels during the test. In fact, decreased C-peptide levels in DAPA-treated mice during the GTT suggested impaired insulin release. Consistent with this, DAPA treatment of Apoe−/−Irs2+/− isolated islets displayed lower glucose-stimulated insulin secretion compared with vehicle-treated islets. Moreover, insulin-signalling experiments showed decreased pAKT activation in DAPA-treated adipose tissue indicating impaired insulin signalling in this tissue. No changes were seen in lesion size, vulnerability or content of macrophages, vascular smooth muscle cells, T cells or collagen. DAPA did not affect circulating inflammatory cells or cytokine levels. Hence, this study indicates that DAPA does not protect against atherosclerosis in insulin-resistant mice in hypercholesterolemic conditions.

Can eosinophils in adipose tissue add fuel to the fire?

In inguinal adipose tissue, beige adipocytes are interspersed among white adipocytes and in close communication with dynamic populations of immune cells. Recent data have demonstrated that anti-inflammatory macrophages (M2) increase thermogenic activity of beige adipocytes, although the mechanism is currently under debate. ILC2, cells via secretion, of methionine enkephalin peptide were found to be able to increase beige thermogenesis. Knights et al. have recently generated a whole-body knock-out of KLF3 (KLF3-/-) to explore its contribution to thermogenesis and weight gain in a diet-induced obesity animal model.

Adipose-specific inactivation of thyroid stimulating hormone receptors in mice modifies body weight, temperature and gene expression in adipocytes.

BackgroundIn obesity, the expression level of thyroid stimulating hormone receptor in adipose tissue is reduced and the levels of thyroid stimulating hormone (TSH) are often elevated within the normal range.Purpose/AimTo investigate the role of TSHR in brown and white adipose tissue (AT) using TSHR knockout (KO) mice and the physiological phenotypes affected by the TSHR knockout.MethodsAT‐specific TSHR KO male mice and wild type (WT) controls were given a high‐fat diet (HFD) or a control diet (CD). Body weights and food consumption were recorded for 20 weeks and body temperatures for the first 3 weeks. At termination, white and brown adipocytes were isolated. Gene expressios was investigated using real‐time PCR. In a subgroup of female KO mice, glucose tolerance was investigated.ResultsTSHR were partially knocked out in KO mice, which gained more weight than WT mice when fed both a CD (p = .03) and HFD (p = .003). Body temperatures were lower in KO mice on CD (p <.001) and on HFD (p <.001) than WT controls. This was in agreement with reduced gene expression of UCP1 in brown adipocytes in the KO mice. Glucose tolerance was significantly impaired in KO mice on CD mice before termination (p <.01). Expression of adipogenic and lipolytic genes were reduced in KO mice, which was exacerbated by HFD. The mRNA levels of adipokines including ADIPOQ and LEP were altered in white adipocytes of KO mice.ConclusionsTSHR KO led to dysfunction of both white and brown AT and predisposition to excess body weight gain in mice. Our data show that TSHR in AT regulates glucose tolerance, lipid metabolism, adipokine profile, and thermogenesis.

Synergistic effect of Lactobacillus gasseri and Cudrania tricuspidata on the modulation of body weight and gut microbiota structure in diet-induced obese mice.

High-fat diet (HFD)-induced obesity has been associated with alteration of gut microbiota alongside body weight gain. In this study, the synbiotic effect of Lactobacillus gasseri 505 (LG) and Cudrania tricuspidata (CT) in HFD-induced mice was revealed. After feeding mice with high-fat diet for 10weeks, combination of LG and CT (LG_CT) exhibited the greatest reduction in the final body weight (11.9%). Moreover, microbial diversity significantly increased, and Principal Coordinate Analysis (PCoA) revealed that the LG_CT group showed closer cluster to NORM. At phylum level, the Firmicutes/Bacteroidetes (F/B) ratio increased in HFD, and the abundance of Bacteroidetes was restored by LG and CT. At genus level, notable changes in Alistipes, Desulfovibrio, Bilophila, and Acetatifactor were observed. Helicobacter elevated to 16.2% in HFD and diminished dramatically to less than 0.01% in LG and/or CT. At species level, L. gasseri increased after the administration of LG (0.54%) and LG_CT (1.14%), suggesting that LG may grow and colonize in the gut and CT can function as a prebiotic. Finally, functional analysis revealed certain metabolic factors correlated with body weight and gut microbiota. This study serves as a potential basis for the application of L. gasseri 505 and C. tricuspidata in the prevention and treatment of diet-induced obesity.Key Points • Combination of L. gasseri (LG) and C. tricuspidata (CT) reduced body weight gain.• Microbial diversity significantly increased in LG_CT treatment.• Abundance of microorganisms involved with leanness increased in LG, CT, and LG_CT.• Body weight is associated with some metabolic functions of gut microbiota.

Relevance of control diet choice in metabolic studies: impact in glucose homeostasis and vascular function

The experimental approach for the study of cardiometabolic disorders requires the use of animal models fed with commercial diets whose composition differs notably, even between diets used for control groups. While chow diets are usually made of agricultural by-products, purified low-fat diets (LF) contain a higher percentage of easy metabolizable carbohydrates, together with a reduced amount of polyunsaturated fatty acids, micronutrients and fiber, all associated with metabolic and vascular dysfunction. We hypothesize that the LF diet, commonly used in control animals, could promote adverse vascular and metabolic outcomes. To address this issue, 5-week-old male C57BL6J mice were fed with a standard (Chow) or a LF diet for 6 weeks. Changes in body weight, adiposity, biochemical parameters, systemic and aortic insulin sensitivity and endothelial function were recorded. LF diet did not modify body weight but significantly impaired systemic glucose tolerance and increased triglycerides and cholesterol levels. Endothelial function and aortic insulin sensitivity were significantly impaired in the LF group, due to a reduction of NO availability. These findings highlight the importance of selecting the proper control diet in metabolic studies. It may also suggest that some cardiometabolic alterations obtained in experimental studies using LF as a control diet may be underestimated.

Neurodegenerative Susceptibility During Maternal Nutritional Programing: Are Central and Peripheral Innate Immune Training Relevant?

Maternal overnutrition modulates body weight, development of metabolic failure and, potentially, neurodegenerative susceptibility in the offspring. Overnutrition sets a chronic pro-inflammatory profile that integrates peripheral and central immune activation nodes, damaging neuronal physiology and survival. Innate immune cells exposed to hypercaloric diets might experience trained immunity. Here, we address the role of maternal overnutrition as a trigger for central and peripheral immune training and its contribution to neurodegeneration and the molecular nodes implicated in the Nod-like receptor protein 3 (NLRP3) inflammasome pathway leading to immune training. We propose that maternal overnutrition leads to peripheral or central immune training that favor neurodegenerative susceptibility in the offspring.

Hypocretin/orexin modulates body weight and the metabolism of glucose and insulin.

The hypocretin/orexin (Hcrt/orexin) unit affects the functions of the nervous, cardiovascular, gastrointestinal, and reproductive systems. Hcrt/orexin ligands and receptors have been localized to different parts of the central and peripheral nervous systems, cerebrospinal fluid and blood, exocrine (pancreas, salivary, lacrimal) as well as endocrine (pancreatic islets, pituitary, adrenal) glands. Several factors including stress, glucagon-like peptide-1 agonists, glutamate, nicotine, glucose, and hypoglycaemia stimulate the expression of Hcrt/orexin system, but it is inhibited by ageing, bone morphogenetic protein, hypoxia/hypercapnia, melanocortin receptor accessory protein 2, and glucagon. Literature reports show that Hcrt/orexin can significantly increase insulin secretion from normal and diabetic rat pancreata. Hcrt/orexin decreases blood glucose concentration and reduces insulin resistance partly via increased tissue expression of glucose transporter type 4. It reduces obesity by increasing browning of fat cells and energy expenditure. Taken together, Hcrt/orexin modulates obesity and the metabolism of glucose and insulin. The Hcrt/orexin system may thus be a target in the development of new therapies for the treatment of diabetes mellitus.

A circadian rhythm-related MTNR1B genetic variant (rs10830963) modulate body weight change and insulin resistance after 9 months of a high protein/low carbohydrate vs a standard hypocaloric diet

Background & aimsThe risk allele (G) of rs10830963 in the melatonin receptor 1 B (MTNR1B) gene presents an association with biochemical parameters and obesity. We study the effect of this SNP on insulin resistance and weight loss secondary to two hypocaloric diets. Methods270 obese subjects were randomly allocated during 9 months (Diet HP: a high protein/low carbohydrate vs. Diet S: a standard severe hypocaloric diets). Anthropometric parameters, fasting blood glucose, C-reactive protein (CRP), insulin concentration, insulin resistance (HOMA-IR), lipid profile and adipocytokines levels were measured. Genotype of MTNR1B gene polymorphism (rs10830963) was evaluated. ResultsAll adiposity parameters, systolic blood pressure and leptin levels decreased in all subjects after both diets. This improvement of adiposity parameters was higher in non-G allele carriers than G allele carriers. After weight loss with Diet HP, (CC vs. CG + GG at 9 months); total cholesterol (delta: −9.9 ± 2.4 mg/dl vs. −4.8 ± 2.2 mg/dl:p < 0.05), LDL-cholesterol (delta: −8.3 ± 1.9 mg/dl vs. −5.1 ± 2.2 mg/dl: p < 0.05), insulin (delta: −4.7 ± 0.8 UI/L vs. −0.9 ± 1.0 UI/L: p < 0.05), triglycerides (delta: −17.7 ± 3.9 mg/dl vs. −6.1 ± 2.8 mg/dl: p < 0.05) and HOMA IR (delta: −0.8 ± 0.2 units vs. −0.2 ± 0.1 units: p < 0.05) improved only in no G allele carriers. After weight loss with Diet S in non G allele carriers, insulin levels (delta (CC vs. CG + GG): −3.4 ± 0.6 UI/L vs. −1.2 ± 0.4 UI/L: p < 0.05), triglycerides (delta: −29.2 ± 3.4 mg/dl vs. −8.2 ± 3.8 mg/dl: p < 0.05), HOMA-IR (delta (CC vs. CG + GG): −1.1 ± 0.2 units vs. −0.1 ± 0.1 units: p < 0.05), total cholesterol (delta: −15.9 ± 7.4 mg/dl vs. −5.8 ± 2.9 mg/dl:ns) and LDL-cholesterol (delta: −13.7 ± 5.9 mg/dl vs. −6.0 ± 2.9 mg/dl: ns) decreased, too. Conclusionsour study detected a relationship of rs10830963 variant of MTNR1B gene with adiposity changes, cholesterol changes and insulin resistance modification induced by two different hypocaloric during 9 months.

Effect of Dietary Calcium on Adipogenesis Program and Its Role in Adipocyte Dysfunction in Male Wistar Rats

Dietary calcium influences obesity-related adipocyte dysfunction by modulating body weight. The molecular mechanism behind this weight management is under intense investigation. In the present study, the authors investigated the effect of dietary calcium on peroxisome proliferator-activated receptor-γ (PPAR-γ)-mediated adipogenesis program and its role in adipocyte dysfunction by measuring the inflammatory and oxidative markers within the adipose tissue of male albino rats. Healthy male rats were fed with a control diet based on AIN-93, and either low-calcium (0.25%) or high-calcium (1.0%) diet for 90 days. A significant inverse (p < 0.05) relationship exists between the calcium intake and anthropometric parameters like adipose tissue mass and body weight. Adipose tissue PPAR-γ activity along with its downstream enzyme activities like glyceraldehydes 3 phosphate dehydrogenase, lipoprotein lipase as well as the protein expression of fatty acid-binding protein 4 and calcium-sensing receptor were significantly increased (p < 0.05) in the low-calcium-fed rats which in turn promoted the adipogenesis program. At the same time, protein expression of inflammatory markers like tumor necrosis factor-α and interleukin-6 and oxidative stress markers like lipid peroxidation and protein carbonylation were significantly increased (p < 0.05) in low-calcium-fed rats. These deleterious effects were suppressed by the high-calcium diet by preventing the activation of the adipogenesis program. Thus, the present study showed the involvement of dietary calcium against the PPAR-γ-mediated adipogenesis program as well as its role in adipocyte dysfunction by regulating the inflammatory and oxidative stress.

Cordycepin Modulates Body Weight by Reducing Prolactin Via an Adenosine A1 Receptor

Cordycepin is an extract from the insect fungus Cordyceps. militaris with various biological function. In previous studies, cordycepin has demonstrated an excellent anti-obesity effect, but the mechanism is unclear. It was also demonstrated that prolactin played an important role in body weight regulation and hyperprolactinemia can promote appetite and accelerate fat deposition. In this study, we explored the molecular mechanism of the anti-obesity effect of cordycepin. In Vivo, the obese rat model was induced by high fat diet for five weeks, and the serum and liver lipid levels coupled with the serum prolactin levels were reduced following cordycepin treatment (P<0.01). The results suggested that cordycepin is a potential drug that lowers blood and liver lipid levels and reduces body weight related to prolactin. Cordycepin also protects adipocytes from enlargement and hepatocytes from lipotoxicity-induced inflammation. In vitro, cordycepin inhibited prolactin secretion in GH3 cells via upregulating the expression of adenosine A1 receptor, and the inhibition effect was blocked by an antagonist of adenosine receptor A1 DPDPX, demonstrating that cordycepin may work as an adenosine agonist. Additionally, cordycepin inhibited the ERK/AKT/PI3K pathway in GH3 cells. At the same time, cordycepin blocked prolactininduced upregulation of lipogenesis genes PRLR, and phosphorylation of JAK2 in 3T3-L1 cells. In an in vivo study, cordycepin downregulated the expression of prolactin receptor (PRLR) but not the phosphorylation of JAK2. Thus, it was proved that cordycepin modulates body weight by reducing prolactin release via an adenosine A1 receptor.

Serum asprosin levels and bariatric surgery outcomes in obese adults.

Asprosin is a novel fasting-induced glucogenic and orexigenic protein hormone. The clinical function of asprosin in obesity is currently unknown. This study investigated the association between asprosin abundance and the outcome of bariatric surgery. Patients with body mass index more than 35 kg/m2 were recruited for the Obesity and Clock for Elegant Aging Registry in 2011-2016. Body weight changes, blood sugar, and asprosin were assessed in 117 patients receiving bariatric surgery and 57 non-obese subjects as normal control. Primary outcomes of excess weight loss percentage at 6 months after bariatric surgery were determined at follow-up. Asprosin levels were significantly higher in obese patients than in non-obese subjects (2360 ± 5094 vs. 307 ± 832 ng/ml, p < 0.0001). Multivariate analyses showed a significant association of asprosin abundance with excess body weight loss percentage at 6 months after surgery (p < 0.0001). After adjusted for age, sex, smoking, HbA1c, cholesterol, and triglyceride, serum asprosin level was the only independent predictor of 6 months excess weight loss percentage after bariatric surgery. Asprosin levels decreased significantly 6 months after bariatric surgery (162.2 ± 169.1 ng/ml). Furthermore, there was no association between asprosin and serum glucose levels in our study. This study provides novel evidence that higher asprosin concentrations before bariatric surgery were associated with the weight reduction magnitude at 6 months after surgery. Further studies are warranted to investigate whether asprosin has direct functions to modulate body weight regulation in humans after bariatric surgery.

Effects of RVD-hemopressin (α) on feeding and body weight after standard or cafeteria diet in rats

Palatability and variety of foods are major reasons for hedonic eating, and hence for obesity. Hemopressin, a hemoglobin α chain-derived peptide, plays antagonist/inverse agonist role on cannabinoid (CB)1 receptors, while RVD-hemopressin(α)[RVD-hp(α)], a N-terminally extended form of hemopressin, has been reported as an allosteric modulator of CB1 and CB2 receptors.We investigated the effects of 14 daily intraperitoneal injections of RVD-hp(α), in Sprague-Dawley rats fed a highly palatable cafeteria-style (CAF) diet (30% fat, 56% carbohydrate, 14% protein; 4.20 kcal/g) compared to standard laboratory chow (STD) food (3.5% fat, 63% carbohydrate, 14% protein, 19.5% other components without caloric value; 3.20 kcal).Food intake, body weight and locomotor activity were recorded throughout the study. Finally, rats were sacrificed and agouti-related peptide (AgRP), neuropeptide Y (NPY), pro-opiomelanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART) and fatty acid amide hydrolase (FAAH) gene expression in the hypothalamus was measured by real-time reverse transcription polymerase chain reaction.We found that CAF diet increased food intake as compared to STD diet. In both STD and CAF diet fed rats, RVD-hp(α) treatment inhibited food intake, increased locomotor activity but did not modify body weight. In vehicle injected animals, CAF as compared to STD diet increased AgRP gene expression. RVD-hp(α) treatment decreased POMC mRNA levels in both diet groups and lowered the elevated AgRP levels induced by CAF diet.RVD-hp(α) treatment plays an anorexigenic role paralleled by increased locomotor activity both in STD and CAF diet fed rats. The inhibition of feeding could be partially mediated by lowering of hypothalamic POMC and AgRP gene expression levels.