I find a Garcinix good number of articles in Obst. Garcinia cambogia for inflammation yearly reward for the best article authored can also incentivize the authors. To publish a journal manuscripts are needed from authors.

Garcinia cambogia for inflammation -

The participants had to undergo strict diets, with 42 of the women ingesting mg capsules of Garcinia cambogia before meals for a total dose of 2. The other participants were given placebos.

Body composition and weight were assessed regularly. Thus, the claims of the effect of increased satiety due to the ingestion of HCA that were noted in animal models were not supported in this human trial. Although Garcinia cambogia, or more specifically, HCA does seem to show some promise with regard to weight loss through reduced food intake and body fat gain by regulating the serotonin levels that are related to satiety feeling satisfied and full after eating , decreased de novo lipogenesis and increased fat oxidation in rats , the evidence of these findings in humans is significantly limited and cannot be considered of clinical relevance at this time.

Diabetes, also known as diabetes mellitus is a disease that occurs when the body does not produce or respond to the hormone insulin efficiently, this results in the abnormal metabolism of carbohydrates which elevates blood glucose levels above what is considered normal.

When we eat carbohydrate-rich food, the sugars and starches are turned into glucose, known as blood glucose when it enters the bloodstream, or blood sugar, this is then used for energy by the cells to function.

The pancreas creates the hormone insulin, this aids in transporting glucose and allows it to enter the cells, effectively acting as a key to the doorway of the cells. When someone has diabetes, their body will either not produce enough insulin or not utilise the hormone effectively.

This causes glucose to accumulate in the blood which can result in a number of health complications such as vision changes, an increased risk of infections developing as the body does not heal as quickly, heart disease or kidney failure. Garcinia cambogia when used as a supplementation in rats to study the effects of the plant on glucose metabolism i.

the way that the body utilises glucose , showed promising results 11 in improving the use of glucose in the body. Human trials conducted set out to prove this theory and the effect of hydroxycitric acid HCA found in Garcinia cambogia in promoting glucose absorption in healthy individuals compared to those with type 2 diabetes.

Type 1 diabetes on the other hand, refers to the inability of the pancreas to produce sufficient insulin if any at all. The randomised controlled trial 12 involved two groups, one made up of twelve healthy individuals and the other eight patients with type 2 diabetes.

Both groups received an infusion of mg of HCA in water over a period of 60 minutes. This was followed by 60 grams of glucose infused over two hours. Blood samples were taken frequently.

The results of the study stated that the healthy individuals who were exposed to HCA showed a slight reduction in the presence of glucose in the blood, known as glycaemia and glucagon a hormone that works with insulin in regulating glucose levels in the body, glucagon raises the concentration of glucose in the bloodstream.

However, no effect was seen on insulin or glucose absorption. HCA did not have any effect on glycemia in those with type 2 diabetes.

The results of the studies done on humans and the effect of Garcinia cambogia on diabetes are not currently very encouraging, however, further large-scaled studies will need to be performed for more accurate and conclusive results to be determined. Until then, it is not recommended that those with diabetes use Garcinia cambogia to treat their condition.

The use of Garcinia cambogia for treating bowel diseases has attracted a large amount of interest due to the plant containing bowel-specific pharmacological properties. Xanthones contained within the plant are powerful antioxidants that are thought to provide gastroprotective effects due to their ability to reduce pain and inflammation.

In a study 1 3 performed in , a research team investigated the anti-inflammatory effect of Garcinia cambogia in rats with colitis. The results from the study showed that the supplementation of Garcinia in colitic rats led to a significant improvement in the symptoms of colitis and damaged caused by it and as such, the plant could potentially provide a new means of treatment for bowel conditions and inflammation.

The main reason for the success of Garcinia cambogia in proving to be a possible means of treatment for inflammatory bowel conditions is due to the plant containing xanthones which inhibit the catalysts or enzymes of inflammation. However, human trials on the success of Garcinia cambogia in reducing inflammation are limited, this makes the findings partial and restrictive to animal models only.

Efficacy of Garcinia Cambogia on Body Weight, Inflammation and Glucose Tolerance in High Fat Fed Male Wistar Rats. Effect of hydroxycitrate on food intake and body weight regain after a period of restrictive feeding in male rats.

Effect of hydroxycitrate on respiratory quotient, energy expenditure, and glucose tolerance in male rats after a period of restrictive feeding. On Aug Dr. S "Journal of Clinical and Diagnostic Research JCDR is a reputed peer reviewed journal and is constantly involved in publishing high quality research articles related to medicine.

Its been a great pleasure to be associated with this esteemed journal as a reviewer and as an author for a couple of years. The editorial board consists of many dedicated and reputed experts as its members and they are doing an appreciable work in guiding budding researchers.

The reviewers provide appropriate suggestions that improve the quality of articles. I strongly recommend my fraternity to encourage JCDR by contributing their valuable research work in this widely accepted, user friendly journal.

I hope my collaboration with JCDR will continue for a long time". S MBBS, MD Pathology , Sanjay Gandhi institute of trauma and orthopedics, Bengaluru. Mamta Gupta, "It gives me great pleasure to be associated with JCDR, since last years. Since then I have authored, co-authored and reviewed about 25 articles in JCDR.

I thank JCDR for giving me an opportunity to improve my own skills as an author and a reviewer. It 's a multispecialty journal, publishing high quality articles. It gives a platform to the authors to publish their research work which can be available for everyone across the globe to read.

For those who have problem in writing manuscript or do statistical work, JCDR comes for their rescue. The journal has a monthly publication and the articles are published quite fast. In time compared to other journals. The on-line first publication is also a great advantage and facility to review one's own articles before going to print.

The response to any query and permission if required, is quite fast; this is quite commendable. I have a very good experience about seeking quick permission for quoting a photograph Fig.

from a JCDR article for my chapter authored in an E book. I never thought it would be so easy. No hassles. Reviewing articles is no less a pain staking process and requires in depth perception, knowledge about the topic for review.

It requires time and concentration, yet I enjoy doing it. The JCDR website especially for the reviewers is quite user friendly. My suggestions for improving the journal is, more strict review process, so that only high quality articles are published. I find a a good number of articles in Obst.

Gynae, hence, a new journal for this specialty titled JCDR-OG can be started. May be a bimonthly or quarterly publication to begin with. Only selected articles should find a place in it. An yearly reward for the best article authored can also incentivize the authors.

Though the process of finding the best article will be not be very easy. I do not know how reviewing process can be improved. If an article is being reviewed by two reviewers, then opinion of one can be communicated to the other or the final opinion of the editor can be communicated to the reviewer if requested for.

This will help one’s reviewing skills. My best wishes to Dr. Hemant Jain and all the editorial staff of JCDR for their untiring efforts to bring out this journal. I strongly recommend medical fraternity to publish their valuable research work in this esteemed journal, JCDR".

Rajendra Kumar Ghritlaharey "I wish to thank Dr. Hemant Jain, Editor-in-Chief Journal of Clinical and Diagnostic Research JCDR , for asking me to write up few words. Writing is the representation of language in a textual medium i e; into the words and sentences on paper.

Quality medical manuscript writing in particular, demands not only a high-quality research, but also requires accurate and concise communication of findings and conclusions, with adherence to particular journal guidelines.

Important Notice. Efficacy of Garcinia Cambogia on Body Weight, Inflammation and Glucose Tolerance in High Fat Fed Male Wistar Rats BFBF Correspondence Dr.

Sridhar Gopalakrishna Magadi, Senior Professor, Department of Biochemistry, Jawaharlal Institute of Postgraduate Medical Education and Research JIPMER , Puducherry – , India. Introduction: Obesity leads to derangements in lipid and glucose homeostasis resulting in various metabolic complications.

Plants containing vital phytochemicals are known to posses anti obesity properties and have proved to exert beneficial effects in obesity.

Objectives: The present study was aimed to investigate the effects of Garcinia Cambogia on body weight, glucose tolerance and inflammation in high fat diet fed male Wistar rats. Body weight, intraperitoneal glucose tolerance test, leptin, tumour necrosis factor-a TNF-a and renal function urea, creatinine, uric acid were studied.

Results: High fat diet fed rats showed increased body weight gain, glucose intolerance, elevated levels of plasma leptin and TNF-a. Supplementation of Garcinia Cambogia extract GE along with high fat diet significantly decreased body weight gain, glucose intolerance, plasma leptin and TNF-a level.

No significant changes were observed in the renal function parameters in any of the groups. Conclusion: Supplementation of the Garcinia Cambogia extract with high fat diet reduced body weight gain, inflammation and glucose intolerance. Users Online : Current Issue Online Ahead of Print Archive Audio-Visual Section Forthcoming Issue.

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Apply as Reviewer Instruction for Reviewer Reviewers Acknowledgment. Simple Search Advanced Search. However, the weight of the visceral WAT including the epididymal, perirenal, retroperitoneal and mesentery WAT was significantly lower in the GC-supplemented mice than in the HFD control mice Figure 1D.

Hence, the weight of the total WAT visceral and subcutaneous WAT was significantly lower in mice fed a GC supplemented HFD. Morphological observations also indicated the epididymal adipocyte size was smaller in the GC-supplemented mice than in the HFD control mice Figure 1E. However, GC supplementation did not alter the extent and degree of fibrosis in the epididymal WAT of HFD-fed mice data not shown.

To examine the mechanism through which GC supplementation reduces the visceral WAT weight, we measured the activity of enzymes that regulate lipid accumulation in visceral WAT. The GC supplementation resulted in a significant decrease in the activity of FAS in the epididymal WAT of mice fed a HFD Figure 2A.

Furthermore, GC-supplemented mice showed a significant increase in the activity of CPT and β-oxidation in the epididymal WAT Figure 2B and C. We also examined the expression of genes that regulate adipogenesis and inflammation. Consistent with the activity of adipose enzymes, GC supplementation significantly down-regulated FAS mRNA expression, whereas it markedly up-regulated CPT mRNA expression in the epididymal WAT of HFD-fed mice Figure 2D.

Moreover, GC-supplemented mice showed a significant increase in the mRNA expression of transcription factor PPARα in the epididymal WAT compared to the control mice. We next determined whether GC influenced HFD-induced glucose intolerance.

The fasting blood glucose, plasma insulin and HOMA-IR levels were not significantly altered by GC supplementation data not shown. However, GC supplementation significantly lowered the blood glucose level compared to the control group at min after glucose loading Figure 3A.

The level of AUC was also markedly decreased in the GC-supplemented mice compared to the control obese mice. No significant differences were observed in the levels of plasma lipids triglycerides, total cholesterol, HDL-cholesterol, phospholipids and free fatty acids and apolipoproteins apolipoproteins A and B between the two groups Table 1.

GC supplementation also did not affect the plasma leptin, TNF-α and MCP-1 levels in the HFD-fed mice; however, it significantly lowered the plasma resistin level Figure 3B and C. Next, we examined the effect of GC supplementation on NAFLD induced by HFD. GC supplementation did not alter the hepatic triglyceride and cholesterol contents as well as the accumulation of hepatic lipid droplets in HFD-fed mice Figure 4A and B.

There were also no significant changes in the activities of hepatic FAS and β-oxidation and in the mRNA levels of the genes involved in lipogenesis and fatty acid oxidation, including FAS, SCD1, CPT, CIDEA, SREBP1c and PPARα, between the two groups Figure 4C and D. However, trichrome staining of the liver revealed GC supplementation increased collagen deposition blue staining compared to the control mice Figure 4E.

Furthermore, Plasma ALT and AST levels were significantly increased in the GC group compared to the control mice Figure 4F.

The mRNA levels of TNF-α and MCP-1, pro-inflammatory markers, were significantly increased in the liver of GC-supplemented mice compared to the control mice Figure 4G.

GC supplementation also caused significant increases of hepatic SOD and glutathione peroxidase GSH-Px mRNA levels as well as TBARS level compared to the control mice, although there was no significant difference in hepatic CAT mRNA level between the two groups Figure 4H and I.

Since unhealthy eating habits combined with limited activity are a major contributor to obesity and its related metabolic disease, lifestyle changes may present a cost-effective first-line of intervention for obesity[ 24 - 26 ].

Dietary supplements seemed to be an inefficient agent for dietary intervention in obese subjects[ 26 ]. However, there are a number of natural dietary supplements for weight management, including GC, guar gum and chitosan[ 34 ].

Among them, HCA-containing GC has been shown to be efficacious in lowering body weight and body fat[ 6 , 10 - 13 ]. But, some clinical trials and animal studies have shown conflicting results[ 6 , 12 ], and a case series on hepatotoxicity has been reported in patients taking GC-containing hydroxycut, although the individual chemical component underling liver injury remains poorly understood[ 14 , 15 ].

Therefore, the aim of this study was first to determine the effects from long-term GC supplementation on obesity and related metabolic diseases as well as the hepatotoxicity in mice fed a HFD.

However, it resulted in significant decreases in visceral WAT weight and adipocyte size in HFD-induced obese mice. The anti-adiposity effect of GC was partly associated with marked decreases in FAS activity and its gene expression in the epididymal WAT.

FAS is a key enzyme involved in de novo fatty acid synthesis and WAT is a major site of fatty acid synthesis and storage. We also found that the activity of CPT as well as fatty acid oxidation in epididymal WAT was elevated by GC supplementation.

Furthermore, the enhanced adipose fatty acid oxidation in GC-supplemented mice was accompanied by the up-regulated mRNA expression of genes involved in fatty acid oxidation such as CPT and PPARα in the epididymal WAT.

The CPT is a major rate-limiting enzyme for fatty acid oxidation, and its gene expression is regulated by PPARα in adipocytes[ 35 ]. The PPARα mRNA expression was decreased in the WAT of both genetic and HFD-induced obese mice, and the down-regulation of PPARα in obese WAT was involved in obesity-induced mitochondrial dysfunction and metabolic disorders[ 36 ].

Taken together, our findings suggest that in HFD-fed mice, a significant reduction in visceral fat accumulation by GC supplementation could be partly due to decreased fatty acid synthesis as well as increased fatty acid oxidation in adipose tissue.

The results of this study are supported by the findings of a previous study which suggested GC supplementation significantly lowered body fat mass, but not body weight and food intake, by inhibiting adipose ATP-citrate lyase ACL activity in Zucker obese rats[ 12 ].

The ACL is another lipogenic enzyme catalyzing the cleavage of citrate to oxaloacetate and acetyl-CoA for de novo fatty acid synthesis[ 37 ].

The inhibitory action of HCA on ACL reduces the acetyl-CoA pool, which can lead to a decreased concentration of malonyl-CoA, a physiological inhibitor of CPT[ 38 ], and thus results in the suppression of body fat accumulation through stimulation of fatty acid oxidation[ 39 ].

Along with the anti-obesity effects of HCA, previous studies have reported on the beneficial effects of HCA on insulin resistance[ 40 , 41 ].

HCA increases the cellular pool of citrate by inhibiting ACL, which in turn can increase glycogen production[ 42 ]. Recently, HCA supplementation enhanced the glycogen synthesis rate in skeletal muscles and improved post-meal insulin sensitivity[ 41 ].

Although we did not measure the level of glycogen in the liver, HCA-containing GC supplementation improved glucose tolerance in HFD-induced obese mice. Furthermore, the plasma resistin level was significantly lowered by GC supplementation in the current study. Resistin is one of the adipokines proposed to link obesity with insulin resistance.

Resistin deficiency ameliorated glucose homeostasis in mice[ 45 ], whereas administration of resistin impaired glucose tolerance and insulin action[ 43 , 46 ]. Thus, the beneficial effect of GC on glucose intolerance might be associated with the decreased resistin level in plasma.

Another mechanism in which GC could contribute to improve glucose tolerance is the lowered body fat mass because excess adiposity, especially in visceral WAT, is considered to promote insulin resistance[ 47 ].

However, there was no significant difference in HOMA-IR which estimates insulin sensitivity from fasting glucose and insulin concentrations. Tripathy et al [ 48 ] reported a significant relationship between hepatic insulin sensitivity and HOMA-IR regardless of the stage of glucose tolerance, suggesting that the HOMA-IR is dependent upon hepatic insulin sensitivity rather than peripheral insulin sensitivity.

Another clinical study also demonstrated that HOMA-IR did not accurately predict insulin sensitivity[ 49 ]. Increased adiposity with the consequences of inflammation and insulin resistance has been linked to the development of NAFLD, which refers to a wide spectrum of liver damage, ranging from simple steatosis to steatohepatitis and cirrhosis.

Steatosis represents the accumulation of fat within the liver through multiple mechanisms including an altered balance in fatty acid uptake and triglycerides secretion, increased de novo lipogenesis, and decreased fatty acid oxidation[ 50 , 51 ]. Steatohepatitis is the combination of steatosis with hepatic inflammation and fibrosis.

Liver fibrosis is excess synthesis and deposition of extracellular matrix proteins including collagen[ 52 ], and pro-inflammatory factors including MCP-1 and TNF-α that contribute to the second hit in the pathogenesis of steatohepatitis.

Among the inflammatory mediators, MCP-1 is a pro-inflammatory chemokine which coordinates leukocyte recruitment to the liver by activation of the CC chemokine receptor 2 CCR2 on inflammatory cells including monocytes and macrophages promoting the inflammatory response[ 53 ].

Several studies indicate that MCP-1 is an important mediator of liver fibrosis[ 54 - 56 ]. MCP-1 mRNA expression was markedly increased in the livers of patients with steatohepatitis and in murine models of steatohepatitis such as mice fed a HFD or methionin-cholin deficient diet[ 57 - 63 ]. CCR2 inhibitor suppressed the early and late features of steatohepatitis including fibrosis[ 64 ], and chronic exposure of HFD induced hepatic MCP-1 mRNA expression in mice before induction of other pro-inflammatory cytokine mRNAs including TNF-α and prior to the onset of steatohepatitis, suggesting that MCP-1 plays a major role in initiating the inflammatory process in steatohepatitis[ 65 ].

Moreover, MCP-1 deficiency reduced liver fibrosis collagen deposition and pro-fibrogenic gene expression in mice fed a methionine-choline deficient diet although it did not affect liver steatosis in this model[ 66 ].

Similarly, we found that GC supplementation did not affect hepatic lipogenesis and lipid droplet formation, but it markedly increased collagen deposition as well as pro-inflammatory MCP-1 and TNF-α mRNA expression in the liver of HFD-fed mice.

Furthermore, GC-supplemented mice exhibited impaired liver function indicated by the elevations of plasma ALT and AST, suggesting that GC possibly promotes liver injury in HFD-fed mice. Several case reports have suggested HCA-containing hydroxycut has potential hepatotoxicity but the underlying mechanism remains unknown[ 14 , 15 , 67 , 68 ].

Our experiments provide new information regarding hepatotoxicity after long-term GC supplementation in HFD-induced obese mice. Accordingly, GC supplementation contributes to steatohepatitis by increasing hepatic collagen accumulation and hepatic MCP-1 and TNF-α expression in mice fed a HFD, which are independent of its effects on HFD-induced hepatic steatosis.

On the other hand, oxidative stress is considered to play an important role in progression of nonalcoholic steatohepatitis and hepatocellular injury[ 69 ]. Reactive oxygen species ROS can damage DNA, lipids and proteins, induce necrosis and apoptosis of hepatocytes and amplifie the inflammatory response.

The ROS also stimulate the production of pro-fibrogenic mediators from Kupffer cells and inflammatory cells and directly induce hepatic stellate cells proliferation, resulting in the initiation of fibrosis[ 70 ].

Antioxidant enzymes such as SOD and GSH-Px ameliorate the damaging effects of ROS. SOD converts superoxide radicals into hydrogen peroxide, which is then further metabolized by GSH-Px, where it catalyzes the destruction of hydrogen peroxide and lipid hydroperoxide.

We observed that the supplementation of GC significantly up-regulated hepatic SOD and GSH-Px mRNA expression with concomitant increase in lipid peroxidation in the liver, suggesting that the increases in antioxidant gene expression by GC seems to be a compensatory response of the liver to cope with oxidative stress.

In conclusion, this study demonstrated that long-term GC supplementation ameliorated adipogenesis in mice fed a HFD by promoting fatty acid oxidation with a simultaneous decrease in fatty acid synthesis in visceral WAT. Furthermore, GC exhibited a protective role against glucose intolerance induced by HFD.

Moreover, this study provides the first evidence that long-term GC supplementation significantly increased hepatic collagen accumulation, lipid peroxidation and MCP-1 and TNF-α mRNA expression as well as plasma AST and ALT levels, thereby contributing partly to the exacerbation of steatohepatitis in HFD-induced obese mice at the doses given.

The observations described above are summarized in Figure 5. Although further research is required to elucidate the efficacy and safety of long-term use of GC in humans, caution is needed when using GC supplements for weight management.

Garcinia Cambogia GC is a popular dietary supplement for weight loss, but the efficacy and hepatotoxicity of long-term GC supplementation remain poorly understood. Thus, authors investigated the long-term supplementation effects of GC on adiposity and non-alcoholic fatty liver disease NAFLD in mice fed a high-fat diet HFD.

A number of experiments reported GC has beneficial effects on weight loss and body fat in some animals and human. However, there are controversial findings and little studies have reported whether these effects persist beyond 13 wk of GC supplementation.

This is first report which shows the supplementation of GC increased hepatic collagen accumulation, inflammatory genes expression and lipid peroxidation as well as plasma alanine aminotransferase and aspartate aminotransferase levels, although HFD-induced hepatic steatosis did not change.

Thus their findings suggest that long-term supplementation of GC induces hepatic fibrosis and inflammation, although it protects against HFD-induced adiposity and glucose intolerance in mice fed a high fat diet. Extensive dietary supplements are popular and widely used for weight management.

However, the optimal dose and safety profiles of many dietary supplements are poorly studied and they are not regulated by the Food and Drug Administration in a manner observed for pharmacological agents. The authors suggest that caution is needed when using GC supplements for weight management, although further research is required to elucidate the efficacy and safety of long-term use of GC in humans.

The authors investigated long-term supplementation effects of GC on adiposity and NAFLD in diet-induced obese mice. They reported that long-term GC supplementation improved adipogenesis by promoting fatty acid oxidation along with a decrease in fatty acid synthesis in visceral white adipose tissue.

They also reported a protective role of GC against glucose intolerance induced by HFD. However, they also showed that long-term GC supplementation increased hepatic collagen accumulation and cytokine expression, thereby exacerbating steatohepatitis.

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Kim YJ, Choi MS, Park YB, Kim SR, Lee MK, Jung UJ. Garcinia Cambogia attenuates diet-induced adiposity but exacerbates hepatic collagen accumulation and inflammation. World J Gastroenterol ; 19 29 : [PMID: DOI: Corresponding Author of This Article. Un Ju Jung, PhD, Center for Food and Nutritional Genomics Research, Kyungpook National University, San-Kyuk Dong, Puk-Ku, Daegu , South Korea.

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World J Gastroenterol. Aug 7, ; 19 29 : Published online Aug 7, doi: Young-Je Kim , Myung-Sook Choi , Yong Bok Park , Sang Ryong Kim , Mi-Kyung Lee , Un Ju Jung.

Young-Je Kim, Myung-Sook Choi, Department of Food Science and Nutrition, Kyungpook National University, Daegu , South Korea. Myung-Sook Choi, Un Ju Jung, Center for Food and Nutritional Genomics Research, Kyungpook National University, Daegu , South Korea.

Yong Bok Park, Sang Ryong Kim, School of Life Sciences and Biotechnology, Kyungpook National University, Daegu , South Korea.

Sang Ryong Kim, Brain Science and Engineering Institute, Kyungpook National University, Daegu , South Korea. Mi-Kyung Lee, Department of Food and Nutrition, Sunchon National University, Jeonnam , South Korea.

Author contributions : Kim YJ and Choi MS contributed equally to this work; Kim YJ performed experiments and analyzed the data; Choi MS designed the study and reviewed and revised the manuscript; Park YB, Kim SR and Lee MK contributed to the critical edition of the manuscript; Jung UJ designed the study, performed experiments, analyzed the data and wrote the manuscript.

Supported by The Basic Science Research Program, No. Correspondence to : Un Ju Jung, PhD, Center for Food and Nutritional Genomics Research, Kyungpook National University, San-Kyuk Dong, Puk-Ku, Daegu , South Korea. Received: March 22, Revised: May 15, Accepted: June 1, Published online: August 7,

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