A high salt diet inhibits obesity and delays puberty in the female rat

Abstract

Background/Objectives Processed foods are considered major contributors to the worldwide obesity epidemic. In addition to high sugar and fat contents, processed foods contain large amounts of salt. Due to correlations with rising adiposity, salt has recently been proposed to be obesogenic. This study investigated three hypotheses: i) high salt contributes to weight gain and adiposity in juvenile female rats, ii) puberty onset would be altered because salt is known to affect neuronal systems involved in activating the reproductive system, and iii) enhanced adiposity will act synergistically with salt to drive early puberty onset. Design Female weanling rats (post-natal day 21, n=105) were fed a low fat/low salt diet, low fat/high salt diet, high fat/low salt diet, or a high salt/high fat diet for 24 days. Metabolic measures, including weight gain, food intake, fecal output, activity, and temperature were recorded in subsets of animals. Results Body weight, retroperitoneal and perirenal fat pad weight, and adipocyte size were all lower in animals fed high fat/high salt compared to animals fed high fat alone. Leptin levels were reduced in high fat/high salt fed animals compared to high fat/low salt fed animals. Daily calorie intake was higher initially but declined with adjusted food intake and was not different among groups after 5 days. Osmolality and corticosterone were not different among groups. Fecal analysis showed excess fat excretion and a decreased digestive efficiency in animals fed high fat/low salt but not in animals fed high fat/high salt. Although respiratory exchange ratio was reduced by high dietary fat or salt, aerobic resting metabolic rate was not affected by diet. High salt delayed puberty onset, regardless of dietary fat content. Conclusions Salt delays puberty and prevents the obesogenic effect of a high fat diet. The reduced weight gain evident in high salt fed animals is not due to differences in food intake or digestive efficiency.

Prevalence of impaired fasting glucose, type 2 diabetes and associated risk factors in undiagnosed Chinese rural population: the Henan Rural Cohort Study

“…The relationship between high salt consumption and development of diabetes has not been established, and it appears its role in diabetes development has not been explored in previous studies. High salt diet has been demonstrated to aid increased lipid absorption in animal studies 36. In our study, however, we found a strong association between high salt diet intake with BMI and WC, possibly suggesting that BMI and WC may mediate the association between high salt intake and diabetes.…”

Test of the hypothesis that eating high-salt food leads to obesity by stimulating sugar-solution consumption

“…Although high-salt diets have been suggested to be obesogenic (e.g., [3,8,23] see introduction), our results are consistent with many other studies that show high-salt diets do not increase body weight or adiposity (e.g., [24][25][26][27]).…”

Analysis of sex differences in dietary copper-fructose interaction-induced alterations of gut microbial activity in relation to hepatic steatosis

“…While the variations of perigonadal white adipose tissue (WAT) weight as well as WAT/body weight ratios were related to dietary copper content in male rats, they were more likely to be affected by dietary fructose in female rats. The energy efficiency ratio (EER, %), i.e., the ratio of body weight gain and total energy intake [ 54 , 55 ], was decreased by dietary fructose in both male and female rats compared to their controls, suggesting the metabolic effects of fructose may not be contributed to the calorie intake. Ad libitum feeding of fructose via drinking water led to a significant increase in water intake and a decrease in pellet food intake.…”