Prolactin stimulates food intake in a dose-dependent manner

Area of Science:

• Endocrinology
• Metabolic Physiology
• Reproductive Biology

Background:

• Lactation in rats is characterized by increased appetite (hyperphagia) and reduced brown adipose tissue (BAT) thermogenesis.
• Previous research suggested a potential role for elevated prolactin levels in mediating these lactation-associated changes.

Purpose of the Study:

• To investigate the dose-dependent effects of exogenous prolactin administration on food intake, BAT mitochondrial function, and body adiposity in female rats.
• To determine if elevated prolactin levels directly stimulate hyperphagia and influence BAT thermogenic capacity independent of lactation.

Main Methods:

• Female rats received daily injections of ovine prolactin at high (3.0 µg/g), medium (1.0 µg/g), or low (0.3 µg/g) doses for 10 days.
• Control groups included rats injected with saline and uninjected rats.
• Measurements included cumulative food intake, body weight gain, and BAT mitochondrial guanosine diphosphate (GDP) binding.

Main Results:

• Prolactin administration led to a significant, dose-dependent increase in cumulative food intake compared to controls.
• Rats treated with prolactin exhibited greater weight gain than control groups.
• No significant differences in BAT mitochondrial GDP binding were observed among any of the experimental groups, indicating unchanged thermogenic capacity.

Conclusions:

• Elevated prolactin levels stimulate food intake in a dose-dependent manner in female rats.
• The observed hyperphagia induced by prolactin is not associated with alterations in brown fat mitochondrial thermogenic capacity.
• Prolactin appears to be a key regulator of appetite during lactation, acting independently of brown fat thermogenesis.