ED Drugs May Help Metabolism and Fat Loss

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The cyclic guanosine monophosphate (cGMP) signaling system is one of the most prominent regulators of many physiopathological processes in humans and rodents. It has been strongly established as an accomplished cellular signal involved in the regulation of energy homeostasis and cell metabolism, and pharmacological enhancement of cGMP has shown beneficial effects in metabolic disorders models. cGMP intracellular levels are finely regulated by phosphodiesterases (PDEs). The main enzyme responsible for the degradation of cGMP is PDE5. Preclinical and clinical studies have shown that PDE5 inhibitors (PDE5i) have beneficial effects on improving insulin resistance and glucose metabolism representing a promising therapeutic strategy for the treatment of metabolic disorders. This review aims to describe the molecular basis underlying the use of PDE5i to prompt cell metabolism and summarize current clinical trials assessing the effects of PDE5i on glucose metabolism.


The increasing prevalence of obesity, type 2 diabetes (T2DM) and other endocrine-metabolic disorders underscores the need to develop new therapeutic strategies [1]. Insulin resistance (IR) has been recognized as the step preceding their development, with diabetes ensuing when insulin secretory capacity fails to compensate for the increased insulin body requirements [2]. Prevention strategies include weight loss and exercise activity but require patients’ compliance and strict adherence; lifestyle interventions are difficult for patients to maintain and the weight loss achieved tends to be regained over time [3]. Pharmacological treatments include metformin and thiazolidinediones, and both drugs demonstrated efficacy in reducing the progression toward diabetes [4,5], but their use is not free of adverse effects [6], although metformin exhibits a safer profile [4]. In this context, one of the promising targets are the second messenger cGMP, whose levels are finely regulated by Phosphodiesterases (PDEs) and, in particular, PDE5. Many authors have investigated the efficacy of PDE5 inhibition in the regulation of glucose and lipid metabolism. PDE5 inhibitors (PDE5i) activity has long been used as an effective treatment for erectile dysfunction and pulmonary hypertension [7,8], and much evidence suggests the efficacy and safety of PDE5i in other pathological conditions, such as cardiovascular diseases [9-11] and endocrine-metabolic disorders [12-14]. Based on recent in vitro and in vivo findings, this review summarizes (i) the molecular mechanisms underlying the effects of PDE5i on glucose and lipid homeostasis (Figure 1) (ii) the data derived from clinical trials assessing possible beneficial effects on humans (Table 1).

*Role of the cGMP-PKG pathway in the control of energy homeostasis

*Effect of PDE5i on adipogenesis and thermogenesis

*Effect of PDE5i on lipolysis

*Effect of PDE5i on energy expenditure and fat oxidation

*Effect of PDE5i on insulin sensitivity and secretion

*Clinical trials


NO-cGMP-PKG signaling pathway plays a pivotal role in the regulation of glucose and lipid metabolism. Although molecular mechanisms are still not completely understood, given the wide expression of PDE5 in metabolic active tissues and the safety of PDE5i, these data suggest that PDE5i may have favorable metabolic effects by improving insulin sensitivity and glucose metabolism before the development of clinical diabetes. This opens a new therapeutic strategy in the prevention of metabolic diseases.


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Metabolic actions of PDE5i in the control of glucose and lipid metabolism.
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Table 2 Metabolic phenotype of mouse models resulting from genetic alteration of cGMP/PKG/PDEs signaling.
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Nelson Vergel

Founder, ExcelMale.com
Wow, I did not know about this research area for PED5 inhibitors. 100 mg/day of Viagra decreased waist circumference (see below).

Nelson Vergel

Founder, ExcelMale.com

PDE5 Inhibition Ameliorates Visceral Adiposity Targeting the miR-22/SIRT1 Pathway: Evidence From the CECSID Trial​

Visceral adiposity plays a significant role in cardiovascular risk. PDE5 inhibitors (PDE5i) can improve cardiac function and insulin sensitivity in type 2 diabetes patients.

To investigate whether PDE5i affect visceral adipose tissue (VAT), specifically epicardial fat (epicardial adipose tissue [EAT]), and what mechanism is involved, using microarray-based profiling of pharmacologically modulated microRNA (miRNAs).

Randomized, double-blind, placebo-controlled study in type 2 diabetes.

Patients and Intervention:
A total of 59 diabetic patients were randomized to receive 100-mg/d sildenafil or placebo for 12 weeks. Fat biopsies were collected in a subgroup of patients. In a parallel protocol, db/db mice were randomized to 12 weeks of sildenafil or vehicle, and VAT was collected.

Main Outcomes and Measures:
Anthropometric and metabolic parameters, EAT quantification through cardiac magnetic resonance imaging, array of 2005 circulating miRNAs, quantitative PCR, and flow cytometry of VAT.

Compared with placebo, sildenafil reduced waist circumference (P = .024) and EAT (P = .045). Microarray analysis identified some miRNAs differentially regulated by sildenafil, including down-regulation of miR-22-3p, confirmed by real-time quantitative PCR (P < .001). Sildenafil's modulation of miR-22-3p expression was confirmed in vitro in HL1 cardiomyocytes. Up-regulation of SIRT1, a known target of miR-22-3p, was found in both serum and sc fat in sildenafil-treated subjects. Compared with vehicle, 12-week sildenafil treatment down-regulated miR-22-3p and up-regulated Sirtuin1 (SIRT1) gene expression in VAT from db/db mice, shifting adipose tissue cell composition toward a less inflamed profile.

Treatment with PDE5i in humans and murine models of diabetes improves VAT, targeting SIRT1 through a modulation of miR-22-3p expression.

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Nelson Vergel

Founder, ExcelMale.com


Active Member
Combining Metformin with Sildenafil

I was just thinking about this combo as I was reading through the material then I got to the bottom of the thread and saw you already had info on it. Ha, ha, good one Nelson!
Interesting about the addition of leucine though.
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