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. Author manuscript; available in PMC: 2016 Mar 13.
Published in final edited form as: Circ Res. 2015 Mar 13;116(6):991–1006. doi: 10.1161/CIRCRESAHA.116.305697

Table 1.

Hemodynamic, neurohumoral, and renal changes in obese humans, compared to lean subjects, and in experimental animal models of obesity caused by a high fat diet

Parameter Humans Dogs Rabbits Rats Mice
Arterial pressure ↑ ↑ ↑ ↑ ↑
Heart rate ↑ ↑ ↑ ↑ ↑
Baroreflex sensitivity ↓ ↓ ↓ ↓ ↓
Cardiac output ↑ ↑ ↑ ↑ ?
VO2 (ml/min) ↑ ↑ ↑ ↑ ↑
VO2 (ml/min/kg body weight) ↓ ↓ ↓ ↓ ↓
Cardiac hypertrophy
 Eccentric ↑ ↑ ↑ ↑ ↑
 Concentric ↑ ↑ ↑ ↑ ↑
Cardiac diastolic function ↓ ↓ ↓ ↓ ↓
Muscle blood flow (resting) ↑ ↑ ↑ ? ?
Muscle blood flow “reserve” ↓ ↓ ? ? ?
GFR* ↑ ↑ ↑ ↑ ↑
Renal blood flow* ↑ ↑ ↑ ↑ ?
Renal Na+ reabsorption ↑ ↑ ↑ ↑ ↑
Sympathetic “activity”#
 Renal ↑ ↑ ↑ ? ?
 Cardiac ↔↓ ? ? ? ?
 Muscle ↑ ? ? ? ?
Plasma insulin ↑ ↑ ↑ ↑ ↑
Insulin sensitivity ↓ ↓ ↓ ↓ ↓
Plasma leptin ↑ ↑ ↑ ↑ ↑

VO2, total body oxygen consumption; GFR, glomerular filtration rate;

*

the GFR and renal blood flow refer to the early phases of obesity before major loss of nephron function has occurred;

#

In some instance, sympathetic “activity” is inferred from indirect measurements such as tissue norepinephrine spillover or from denervation studies; plasma insulin and leptin concentrations refer to fasting levels.