Category Archives: Obesity

Renal Effects of Chronic Pharmacological Manipulation of CB2 in Rats with Diet Induced Obesity.

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“In diabetic nephropathy CB2 agonism reduces albuminuria and podocyte loss; however the role of CB2 in obesity-related nephropathy is unknown. The aim of this study was to determine the role of CB2 in a model of diet-induced obesity (DIO)…

This study demonstrates that while agonism of CB2 with AM1241 treatment for six weeks does not reduce weight gain in obese rats, it leads to improvements in obesity related renal dysfunction.”

http://www.ncbi.nlm.nih.gov/pubmed/25537025

“Alexandros Makriyannis is a professor in the Department of Medicinal Chemistry at Northeastern University, where his research group has synthesized many new compounds with cannabinoid activity.

Chronic administration with AM251 improves albuminuria and renal tubular structure in obese rats.

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“Modulation of the endocannabinoid system as an anti-obesity therapeutic is well established, however the direct effects of CB1 antagonism on renal function and structure in a model of diet-induced obesity (DIO) are unknown. The aim of this study was to characterise the renal effects of the CB1 antagonist AM251 in a model of DIO.

Antagonism of CB1 with AM251 significantly reduced weight gain, systolic blood pressure, plasma leptin, and reduced albuminuria and plasma creatinine levels in obese rats.

Importantly, there was a significant reduction in tubular cross-section diameter in the obese rats treated with AM251. An improvement in albuminuria was likely due to the reduction in tubular size, reduced leptinemia and maintenance of megalin expression levels. In obese rats, AM251 did not alter diastolic blood pressure, sodium excretion, creatinine clearance or expression of the fibrotic proteins VEGF, TGFb1 and collagen IV in the kidney.

This study demonstrates that treatment with CB1 antagonist AM251 improves renal outcomes in obese rats.”

http://www.ncbi.nlm.nih.gov/pubmed/25804605

“Alexandros Makriyannis is a professor in the Department of Medicinal Chemistry at Northeastern University, where his research group has synthesized many new compounds with cannabinoid activity… AM-251 — an inverse agonist at the CB1 cannabinoid receptor that is structurally related to SR141716A (rimonabant), but has a higher binding affinity with a Ki value of 7.5nM.”  http://en.wikipedia.org/wiki/List_of_AM_cannabinoids

In Vivo imaging of the cannabinoid CB1 receptor with positron emission tomography.

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“Positron emission tomography (PET) can visualize and quantify receptors and other targets in the living human brain, and recent progress in radioligand development has enabled measurement of cannabinoid CB1 receptors. Cannabinoid CB1 receptors have been implicated in multiple human diseases, such as obesity, mood disorders, and addiction. First in vivo human studies have shown distinctive spatial and temporal alterations in cannabinoid CB1 receptor binding in addictive disorders.”

http://www.ncbi.nlm.nih.gov/pubmed/25788235

Cannabis use in relation to obesity and insulin resistance in the inuit population.

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“OBJECTIVE:

To ascertain the relationship between cannabis use, obesity, and insulin resistance…

Cannabis use was highly prevalent in the study population and was statistically associated with lower body mass index (BMI)

CONCLUSIONS:

Cannabis use was associated with lower BMI, and such an association did not occur through the glucose metabolic process or related inflammatory markers. The association between cannabis use and insulin resistance was mediated through its influence on weight.”

http://www.ncbi.nlm.nih.gov/pubmed/25557382

Two non-psychoactive cannabinoids reduce intra-cellular lipid levels and inhibit hepatosteatosis.

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“Obesity and associated metabolic syndrome have quickly become a pandemic and a major detriment to human health globally.

The presence of non-alcoholic fatty liver disease (NAFLD; hepatosteatosis) in obesity has been linked to the worsening of the metabolic syndrome, including the development of insulin resistance and cardiovascular disease. Currently, there are few options to treat NAFLD, including life style changes and insulin sensitizers.

Recent evidence suggests that the cannabinoids Δ9-tetrahydrocannabivarin (THCV) and cannabidiol (CBD) improve insulin sensitivity; we aimed at studying their effects on lipid levels…

THCV and CBD directly reduce accumulated lipid levels in vitro in a hepatosteatosis model and adipocytes.

…these cannabinoids are able to increase yolk lipid mobilization and inhibit the development of hepatosteatosis respectively.

CONCLUSIONS:

Our results suggest that THCV and CBD might be used as new therapeutic agents for the pharmacological treatment of obesity- and metabolic syndrome-related NAFLD/hepatosteatosis.”

http://www.ncbi.nlm.nih.gov/pubmed/25595882

http://www.thctotalhealthcare.com/category/obesity-2/

Neural Effects of Cannabinoid CB1 Neutral Antagonist Tetrahydrocannabivarin (THCv) on Food Reward and Aversion in Healthy Volunteers.

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“Disturbances in the regulation of reward and aversion in the brain may underlie disorders such as obesity and eating disorders.

We previously showed that the cannabis receptor (CB1) inverse agonist rimonabant, an anti-obesity drug withdrawn due to depressogenic side effects, diminished neural reward responses yet increased aversive responses. Unlike rimonabant, tetrahydrocannabivarin (THCv) is a neutral CB1 receptor antagonist and may therefore produce different modulations of the neural reward system…

Conclusions: Our findings are the first to show that treatment with the CB1 neutral antagonist THCv increases neural responding to rewarding and aversive stimuli.

This effect profile suggests therapeutic activity in obesity, perhaps with a lowered risk of depressive side effects.”

http://www.ncbi.nlm.nih.gov/pubmed/25542687

http://www.thctotalhealthcare.com/category/obesity-2/

The interface: marijuana and body weight.

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“Acute marijuana use is classically associated with snacking behavior (colloquially referred to as “the munchies”). In support of these acute appetite-enhancing effects, several authorities report that marijuana may increase body mass index in patients suffering from human immunodeficiency virus and cancer…

Marijuana is a clinically controversial substance, but one potential medical benefit may be weight gain. According to available studies, appetite stimulation as well as weight gain may occur in patients with physical debilitation due to HIV/AIDS and/or cancer.

As for the effects of marijuana on body weight in the general population, use appears to be associated with a lower body mass index.

…marijuana may genuinely be a regulatory compound, increasing weight in those with low weight, but not in those who are normal or overweight.”

 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4204468/

[Importance of the endocannabinoid system in the regulation of energy homeostasis].

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“The endocannabinoid system is an endogenous signaling system that plays a role in the regulation of energy homeostasis and lipid and glucose metabolism-all of which can influence cardiometabolic risk. The endocannabinoid system appears to be a promising novel mechanistic pathway that modulates important aspects afcardiovascular and metabolic function. The endocannabinoid system is normally a silent physiologic system that becomes transiently activated, that is, only when needed. Evidence suggests that the endocannabinoid system is tonically overactive in human obesity and in animal models of genetic and diet-induced obesity. However, there is evidence in studies that the ECS is tonically overactivated in obesity, although it remains unclear whether overactivation of the ECS precedes or is consequent to expression of the obese phenotype. Rimonabant, a selective cannabinoid-1 receptor (CB1) blocker, has been shown to reduce smoking, body weight and improve and improves the profile of several metabolic risk factors in high-risk patients.”

http://www.ncbi.nlm.nih.gov/pubmed/23687711

http://www.thctotalhealthcare.com/category/obesity-2/

Mitochondria: A Possible Nexus for the Regulation of Energy Homeostasis by the Endocannabinoid System?

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“The endocannabinoid system (ECS) regulates numerous cellular and physiological processes through the activation of receptors targeted by endogenously produced ligands called endocannabinoids. Importantly, this signalling system is known to play an important role in modulating energy balance and glucose homeostasis. For example, current evidence indicates that the ECS becomes overactive during obesity whereby its central and peripheral stimulation drives metabolic processes that mimic the metabolic syndrome. Herein, we examine the role of the ECS in modulating the function of mitochondria which play a pivotal role in maintaining cellular and systemic energy homeostasis, in large part due to their ability to tightly coordinate glucose and lipid utilisation. Because of this, mitochondrial dysfunction is often associated with peripheral insulin resistance and glucose intolerance, as well as the manifestation of excess lipid accumulation in the obese state. This review aims to highlight the different ways through which the ECS may impact upon mitochondrial abundance and/or oxidative capacity, and where possible, relate these findings to obesity-induced perturbations in metabolic function. Furthermore, we explore the potential implications of these findings in terms of the pathogenesis of metabolic disorders and how these may be used to strategically develop therapies targeting the ECS.”

http://www.ncbi.nlm.nih.gov/pubmed/24801388

http://www.thctotalhealthcare.com/category/obesity-2/

Obesity and cannabis use: results from 2 representative national surveys.

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“We hypothesized that the prevalence of obesity would be higher in cannabis users than in nonusers… this analysis showed that even if cannabis consumption increases appetite, people using cannabis are less likely to be obese than people who do not use cannabis…

The authors conclude that the prevalence of obesity is lower in cannabis users than in nonusers.”

http://www.ncbi.nlm.nih.gov/pubmed/21868374
http://aje.oxfordjournals.org/content/174/8/929.long