Androgens Are Necessary For The Development Of Fructose-induced Hypertension

thyrulian

Member
Joined
Mar 20, 2015
Messages
114
http://www.ncbi.nlm.nih.gov/pubmed/14757778

Hyperinsulinemia and insulin resistance are closely associated with hypertension in humans and in animal models. Gender differences have been found in the development of hypertension in fructose-fed rats. The objectives of the present study were, first, to clarify whether androgens are required in the development of hyperinsulinemia, insulin resistance, and hypertension in fructose-fed rats, and second, to determine if cyclooxygenase-1 and cyclooxygenase-2 are also increased in the arteries of these rats. Male rats were gonadectomized or sham-operated and fed a 60% fructose diet beginning at age 7 weeks. Blood pressure was measured by a tail-cuff method, and an oral glucose tolerance test was performed to assess insulin sensitivity after 8 weeks of fructose feeding. Cyclooxygenase-1 and cyclooxygenase-2 mRNA expression was also assessed in the thoracic aortae and mesenteric arteries. Gonadectomy prevented hypertension from developing in the fructose-fed rats, but hyperinsulinemia and insulin resistance developed. There was an increase in cyclooxygenase-2 expression in the thoracic aortae and mesenteric arteries of the fructose-fed sham-operated rats while the expression of cyclooxygenase-1 remained unchanged. Gonadectomy prevented the mRNA overexpression of vascular cyclooxygenase-2 in the fructose-fed rats. These results suggest that the presence of androgens is necessary for the development of fructose-induced hypertension. Androgens apparently act as a link between hyperinsulinemia/insulin resistance and hypertension in fructose-hypertensive rats. Furthermore, an increase in the expression of cyclooxygenase-2 is implicated in the development of hypertension. The mechanisms involved require further study.

But fret not! Our ever-reliable (and in no way ever harmful) buddies acetylcholine and nitric oxide can protect us!

But... hang on, surely our bestie's got our back!? :pray

[Estrogen] found to "protect" against "harmful" effects of fructose

Yes! I knew it!

:claporange
 

Wagner83

Member
Joined
Oct 15, 2016
Messages
3,295
There are a few studies out there with fructose and hypertension.
I'm myself not feeling well at the moment on a peatish diet (good amount of fructose in the form of juices, sucrose and some starches + lots of calcium from dairy), I feel tensed and uneasy in the torso (particularly lower left side) and with some pressure in the back of the head, sleep was disturbed too. I did not measure blood pressure so can't assert it's the reason behind the symptoms.

https://www.hindawi.com/journals/ijn/2011/315879/
The mechanism of hypertension in response to fructose is complex but appears to be mediated by increased sodium absorption in the intestine, by inhibition of systemic endothelial function, and by stimulation of the sympathetic nervous system [14, 43, 44] (Figure 1). In addition, some of the effect of fructose to increase blood pressure may be the consequence of fructose-induced increases in intracellular and serum uric acid. First, fructose-induced hypertension in rats is largely ameliorated by lowering uric acid levels [40]. Second, in one study in overweight men, the rise in ambulatory blood pressure in response to 200 g of oral fructose per day for two weeks was blocked in those subjects concomitantly administered allopurinol [26].

2.5. Kidney Disease

Fructose and sucrose are also known to induce renal hypertrophy and tubulointerstitial disease in rats [10, 45, 46]. The mechanism may involve two central pathways (Figure 2). First, the rise in uric acid in response to uric acid may cause an afferent arteriolopathy resulting in glomerular hypertension [40]. Second, fructose may also be filtered into the urine where it is taken up in the S3 segment of the proximal tubule, leading to local intracellular generation of uric acid with oxidative stress and local inflammation [8].

The administration of fructose to rats with reduced renal function (the remnant kidney model) can accelerate the progression of renal disease, resulting in worse proteinuria, glomerulosclerosis, and tubulointerstitial fibrosis [47]. Fructose intake also impairs calcium absorption and reduces 25-OH Vitamin D and 1,25-dihydroxy Vitamin D levels in this model [48]. Furthermore, the intake of sugary soft drinks in humans is associated with increased prevalence of albuminuria [49]. Our group has also recently administered a low-fructose diet to subjects with stable chronic kidney disease for a period of 6 weeks. While we observed no effect on renal function during the period of the study, we did observe a reduction in inflammatory markers and a fall in blood pressure in subjects with the “dipper” physiology (i.e., those subjects whose blood pressure spontaneously falls at night during sleep) [49]. Clearly further studies are needed to determine if limiting added sugars may benefit subjects with kidney disease.

This (bold) could be an other reason for feeling bad, if the diet is high in calcium and it can't get absorbed results won't be posititive.

2.6. Role of Natural Fruits

While much work has focused on fructose as driving obesity, insulin resistance, and cardiorenal disease, not all fructose sources may be the same. Thus, natural fruits also are rich in antioxidants, ascorbate, polyphenols, potassium, and fiber that may counter the effects of fructose [13, 50]. Indeed, Forman et al. [51] reported that fructose intake did not correlate with elevated blood pressure in a population in which much of the fructose intake was from fruit, whereas Jalal et al. [37] found a strong association of fructose intake with blood pressure when the fructose content from natural fruits was excluded.

I find this quote particularly interesting, I do not know how it would apply to juices, especially non fresh pressed juices.

2.7. Caveats

While there is increasing evidence for a role for fructose as a contributory factor to obesity and metabolic syndrome, most of the data has relied on epidemiological studies, experimental models, and cell culture. In contrast, studies in which fructose or sucrose is administered to subjects have shown variable effects on metabolic parameters. In general, few metabolic effects are observed with fructose when it is given to young, healthy, and lean subjects [52–54]. This contrasts with studies in overweight/obese or insulin-resistant subjects in which metabolic effects from fructose or sucrose are commonly observed [22, 26, 55–58]. One potential explanation may relate to the absorption of fructose, which is known to increase with fructose exposure [59, 60]. Fructose effects are also potentiated by glucose [61, 62], and most studies have only examined fructose alone. Most studies also show, both in animals and humans, that the effects of fructose are greater on postprandial lipids, fatty liver, and insulin resistance rather than on weight gain per se. Indeed, the effects of fructose may be more on inducing leptin resistance, and it may require the addition of high-fat diet to show the weight gain [35]. More studies are necessary before firm conclusions can be made. Nevertheless, the evidence that excessive intake of fructose may have multiple adverse effects on human health seems to be mounting.
 
Last edited:

Similar threads

Back
Top Bottom