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If you have too much glucose in your blood, your body produces less testosterone. The mechanism involved has been shown in an in-vitro study published by Italian endocrinologists at the University of Florence in the International Journal of Endocrinology. If you want to boost your testosterone level in a natural way, make sure you don’t develop Type-2 diabetes and avoid extremely high glucose peaks.

If you have too much glucose in your blood, your body produces less testosterone. The mechanism involved has been shown in an in-vitro study published by Italian endocrinologists at the University of Florence in the International Journal of Endocrinology. If you want to boost your testosterone level in a natural way, make sure you don’t develop Type-2 diabetes and avoid extremely high glucose peaks.

The Italians did the study because they wanted to better understand why diabetes sufferers often produce little testosterone, as a result of which they may develop sexual problems or infertility. They experimented with human cells that produce the gonadotropin-releasing hormone [GnRH]. GnRH [structural formula shown below] plays a key role in the body’s release of testosterone.

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In the brain the hypothalamus releases GnRH a couple of times a day. This hormone then stimulates the release of two other hormones in the pituitary: LH and FSH. These hormones in turn are responsible for testosterone production in the testes in men and the production of testosterone, progesterone and estradiol in the ovaries in women.

The researchers exposed GnRH-producing cells to a normal concentration of glucose [5 millimoles] [NG], a high concentration of glucose [22 millimoles] [HG], a very high concentration of glucose [40 millimoles] [VHG] and to the carbohydrate mannitol in a concentration of 20 millimoles [M].

If your glucose and insulin regulation is working ok your glucose levels won’t reach the high levels the Italians used in their experiment. Diabetics on the other hand may experience these levels. And foods containing large amounts of rapidly absorbed carbohydrates can boost healthy people‚Äôs glucose levels to somewhere between the normal concentration [5 millimoles] [NG] and the high concentration [20 millimoles] [HG].

The figures below show that high concentrations of glucose reduce the release of GnRH. This is probably because, in large quantities, glucose reduces the production of the receptor for the KISS-1 peptide as well as the release of KISS-1. KISS-1 is really a hormone and it boosts the release of GnRH.

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A high concentration of glucose also reduces the manufacture of leptin [LEPR] receptors, as is shown above. Leptin is a hormone released by fat cells. It stimulates the release of LH, and therefore also testosterone, via KISS-1.

The Italians tested their theory by exposing their GnRH-producing cells to synthetic leptin. The figure below shows that high concentrations of glucose inhibited the production of GnRH through leptin.

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“Even if obtained in vitro, our findings support the idea of a deleterious direct contribution of hyperglycemia on human GnRH neurons, thus providing new insights into the pathogenic mechanisms linking hypogonadotropic hypogonadism to metabolic disorders”, the researchers write.

The Italians are not a hundred percent sure of their findings: and therefore whether what they observed in the cells they used is representative of what happens to all GnRH-producing cells in the brain.

The Italians’ research was not funded by a low-carb diet products manufacturer but by the Italian government.

Negative effects of high glucose exposure in human gonadotropin-releasing hormone neurons.

Abstract

Metabolic disorders are often associated with male hypogonadotropic hypogonadism, suggesting that hypothalamic defects involving GnRH neurons may impair the reproductive function. Among metabolic factors hyperglycemia has been implicated in the control of the reproductive axis at central level, both in humans and in animal models. To date, little is known about the direct effects of pathological high glucose concentrations on human GnRH neurons. In this study, we investigated the high glucose effects in the human GnRH-secreting FNC-B4 cells. Gene expression profiling by qRT-PCR, confirmed that FNC-B4 cells express GnRH and several genes relevant for GnRH neuron function (KISS1R, KISS1, sex steroid and leptin receptors, FGFR1, neuropilin 2, and semaphorins), along with glucose transporters (GLUT1, GLUT3, and GLUT4). High glucose exposure (22?mM; 40?mM) significantly reduced gene and protein expression of GnRH, KISS1R, KISS1, and leptin receptor, as compared to normal glucose (5?mM). Consistent with previous studies, leptin treatment significantly induced GnRH mRNA expression at 5?mM glucose, but not in the presence of high glucose concentrations. In conclusion, our findings demonstrate a deleterious direct contribution of high glucose on human GnRH neurons, thus providing new insights into pathogenic mechanisms linking metabolic disorders to reproductive dysfunctions.

PMID: 24489542 [PubMed] PMCID: PMC3893744

Source: http://www.ncbi.nlm.nih.gov/pubmed/24489542

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