Following sex hormone withdrawal, sexual dimorphism occurs in obese rats.

Differences in insulin resistance development due to sex hormone deprivation

A decrease in plasma testosterone (Table 4) confirmed that sex hormone shortage occurred at week 4. 1) or estradiol (Table 2) levels. When compared to sex-matched NDS at similar time points, orchiectomized and ovariectomized animals in both dietary groups M-ORX, F-OVXX, F-HFO, and F-HFO had significantly lower plasma testosterone or estradiol levels. M-HFS and FHFS had significantly higher body weights than sex-matched NDS. M-NDS had a lower body weight, food intake, visceral fat, and body weight than M-ORX. The metabolic parameters of M-ORX and M-HFS, F-OVX, M–HFO, F–OVX, F–HFS, F-HFO, and F-HFO were not different from sex-matched NDS (Tables). 35).

Table 1 Summary of blood testosterone levels
Table 2 Summary of blood serum estrogen levels
Table 3: Effects of sexhormone on metabolic parameters in normal diet-fed males and female rats
Table 4: Effects of diet on metabolic parameters in males and female rats
Table 5: Effects of dietary intake and sex hormone deprivation upon metabolic parameters in male rats and female rats

The results for week 8 were the same as those for week 4. In contrast, the body weight, food consumption and visceral fatty mass of MORX were not affected by week 8. F-OVX, on the other hand, had a significantly higher body weight than F-NDS. M-ORX did develop peripheral insulin resistance but it was not detected in FOVX or the HFD groups (M–HFS, M–HFO, F–HFS, F-HFS and F-HFO). This was confirmed by higher levels of insulin (Tables). 35).

The results of week 12 were very similar to those of week 8. F-OVX had significantly more visceral fat than the F-NDS, but this was not the case for the age-matched M-ORX. M-ORX developed no peripheral insulin resistance during week 12. F-OVX and HFD-treated F-HFO-treated rats (MHFS/M-HFO/F-HFS/F-HFO and F) still showed consistent impairments of metabolic parameters compared with sexmatched NDS rats. (Tables 35). M-HFS also had a markedly higher body mass than M–NDS. However the body weight and visceral weight mass of the orchiectomized rats M-ORX (and M–HFO) were not affected or decreased compared to M–NDS (Tables). 35).

Differences in the development and progression of oxidative Stress in the presence sex hormone deprivation

M-ORX and MFO groups had significantly higher serum and cardiac MDA at week 4 than the age-matched NDS group (Tables 3 5). Moreover, both serum and cardiac MDA were significantly higher at week 8 in M–ORX, M–HFS, M–HFO, and F–HFO groups compared to the age-matched ND (Tables). 35). M-ORX, MHFS and M–HFO were all significantly higher in week 12 than the age-matched NDS (Tables). 35).

Differences in the development and severity of HRV impairment and cardiac dysfunction in the presence sex hormone deprivation

For the LV contractile functions of male rats, a marked drop in %EF was observed at week 4, and continued to decline by weeks 8 through 12, in both M-ORX- and M-HFO groups (Fig. 1A–C). M-HFS showed a significant decrease in %EF after weeks 8 and 12, when compared to MORX and MHFO groups. 1B, C).

Fig. Fig.
figure 1

AThe LV function at four weeks BThe LV function at 8 Weeks CThe LV function at twelve weeks. *P < 0.05 vs sex-matched ND-Sham (n = 6/group). P < 0.05 vs male orchiectomized rats (n = 6/group). P < 0.05 vs female high-fat diet-fed ovariectomized rats (n = 6/group). S sham, ND normal diet, HFD high-fat diet, ORX orchiectomized rats, OVX ovariectomized rats.

The %EF of female rats was the same for F-OVX as F-NDS, but it was significantly lower in F-OVX than F-NDS (Fig. 1A, B). However, F-HFO group showed a significant decrease in %EF starting at week 8 (Fig. 1B). Fig. 12. 1C). A statistically significant interaction between gender, hormone, and food was not found at week 4 of the LV function. F(1, 16) = 4.268, P = 0.06. However, there was a statistically significant interaction between gender, hormone, and food at week 8.F(1, 16) = 18.626, P = 0.001) and week 12 (F(1, 16) = 18.445, P = 0.001).

In accordance with the %EF profiles, impaired cardiac autonomic balance first was detected in both the M-ORX- and M-HFO groups (Fig. 2A). Moreover, the ratio LF/HF in M-ORX and M–HFO groups significantly increased from week 4, compared to the M-NDS group. In addition, the M-HFS group showed cardiac autonomic dysregulation between weeks 8 and 12. (Fig. 2B, C).

Fig. 2: Effect of sex hormone and dietary intake on LF/HF ratio at various time courses (4-8 and 12 weeks).
figure 2

AThe LF/HF ratio at four weeks BThe LF/HF ratio at 8 Weeks. CThe LF/HF ratio at 12 Weeks. *P < 0.05 vs sex-matched ND-Sham (n = 6/group). *P < 0.05 vs sex-matched ND-Sham (n = 6/group). P < 0.05 vs male orchiectomized rats (n = 6/group). P < 0.05 vs female high-fat diet-fed ovariectomized rats (n = 6/group). S sham, ND normal diet, HFD high-fat diet, ORX orchiectomized rats, OVX ovariectomized rats.

At week 4, in female rats, the cardiac autonomic control was not different between groups (Fig. 2A). However, the only group with a lower HRV was found at week 8 was the F-HFO (Fig. 2B), suggesting that the impaired cardiac autonomic regulation was firstly developed in the F-HFO group. Fig. 12 shows that F-OVX, F–HFS, and F-HFO groups had a higher LF/HF ratio than the F-NDS age-matched group (Fig. 2). Week 12 saw a significant increase in the ratio LF/HF in F-HFO rats (Fig. 2C). Only week 8 of the LF/HF ratio revealed a statistically significant three-way interaction among gender, food, hormones. F(1, 16) = 6.129, P = 0.025.

In the presence of sex hormone shortage, there are differences in the development and progression of cardiac mitochondrial dysfunction.

A decreased cardiac mitochondrial function in male rats exposed to sex hormone deprivation, M-ORX or M-HFO, was detected as early as week 4, and continued through weeks 8 and 12, as evidenced by an increased level of mitochondrial ROS (Fig. 3), mitochondrial depolarization (Fig. 4), and mitochondrial swelling (Fig. 5) when compared with age-matched M-NDS. The M-HFS group had cardiac mitochondrial dysfunction detected at week 8 (Figs. 3B, 4B, 5B).

Fig. 3: Effect of sex hormone and dietary intake on cardiac mitochondrial ROS levels at different time periods (4, 8, and 12-weeks).
figure 3

AThe cardiac mitochondrial ROS level after 4 weeks BThe cardiac mitochondrial ROS level after 8 weeks CThe cardiac mitochondrial ROS level after 12 weeks. *P < 0.05 vs sex-matched ND-Sham (n = 6/group). *P < 0.05 vs sex-matched ND-Sham (n = 6/group). P < 0.05 vs male orchiectomized rats (n = 6/group). P < 0.05 vs female high-fat diet-fed ovariectomized rats (n = 6/group). S sham, ND normal diet, HFD high-fat diet, ORX orchiectomized rats, OVX ovariectomized rats.

Fig. Fig.
figure 4

AThe cardiac mitochondrial membrane has undergone depolarization for 4 weeks. BThe 8-week mark marks the beginning of cardiac mitochondrial membrane polarization. CThe cardiac mitochondrial membrane depolarization at 12 weeks. *P < 0.05 vs sex-matched ND-Sham (n = 6/group). P < 0.05 vs male orchiectomized rats (n = 6/group). S sham, ND normal diet, HFD high-fat diet, ORX orchiectomized rats, OVX ovariectomized rats.

Fig. Fig.
figure 5

AThe cardiac mitochondrial swelling after 4 weeks BThe 8-week mark of cardiac mitochondrial swelling CThe 12-week mark is the cardiac mitochondrial swelling. *P < 0.05 vs sex-matched ND-Sham (n = 6/group). *P < 0.05 vs sex-matched ND-Sham (n = 6/group). P < 0.05 vs male orchiectomized rats (n = 6/group). P < 0.05 vs female high-fat diet-fed ovariectomized rats (n = 6/group). S sham, ND normal diet, HFD high-fat diet, ORX orchiectomized rats, OVX ovariectomized rats.

Figs. 4 shows that the surrogate for cardiac mitochondrial function was not different in female rats (Figs. 3A, 4A, 5A). Only the F-HFO group had impaired cardiac mitochondrial function at week 8 (Figs). 3B, 4B, 5B). Interestingly, F-OVX and FHS rats both showed cardiac mitochondrial dysfunction by week 12 (Figs. 3C, 4C, 5C). Additionally, the cardiac mitochondrialROS production. We found no statistically significant three-way interaction of gender, food, and hormone at week 4. F(1, 16) = 2.027, P = 0.174. However, there was statistically significant interaction between hormones, gender, and food at week 8.F(1, 16) = 7.742, P = 0.013) and week 12 (F(1, 16) = 12.981, P = 0.002). Interestingly, there was no statistically significant interaction between gender, food, and hormone at any time point in the alteration of cardiac mitochondrial membrane potential. Only week 8 showed a statistically significant three way interaction between gender, hormone, and food in relation to cardiac mitochondrial swelling. F(1, 16) = 10.957, P = 0.004.

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