The excess body fat of obese horses promotes inflammation through its secretion of substances known as cytokines. Cytokines can damage the areas within the hypothalamus that recognize leptin. Leptin is high, but the brain is not responding to it. The result? The appetite does not decrease; instead the horse keeps on eating, getting more obese, producing more cytokines, increasing inflammatory damage to the hypothalamus, resulting in greater leptin resistance.
The leptin resistant horse will, first and foremost, have excess body fat. His appetite will seem insatiable and he will rarely lift his head from eating. His metabolic rate is sluggish, causing him to pack on the pounds very easily. He is reluctant to move and his energy level is low.
Morrison, C. D., Huypens, P., & Stewart, L., (2009), Implications of crosstalk between leptin and Insulin signaling during the development of diet-induced obesity,
The proposed link between the hypothalamus and obesity and the related studies can be very useful if a control can be formulated to maintain healthy level of leptin in the blood stream. A possible chemical control to obesity and other dietary diseases such as diabetes could prove invaluable with the current increase in prevalence of overweight individuals. However, a change in lifestyle and nutritional habits is necessary in order to ensure the control of obesity and other cases of problems resulting from being overweight in the meantime.
The research on leptin has received much support in the recent past with some propositions being made on its development as opposed to earlier notions of obesity surgery or radiotherapy which were considered more controversial. However, until such studies are successful, human beings will have to contend with the use of diets and regular exercise in order to control their weight and maintain good health. By using such traditional methods, it is hoped that long-term feeding behavior can be maintained and obesity avoided altogether.
As a result of such research efforts and the associated inferences, various assertions have been presented to explain the regulatory control of the hypothalamus on food intake. These include the presupposition that gastrointestinal hormones, or gut-peptides, are responsible for the reticence to food intake. As food enters the gastrointestinal tract, it stimulates the secretion of these hormones to the brain consequently inducing a feeling of fullness. Another hypothesis is that of glucose use by the neurons found in the ventromedial nuclei. This glucostatic approach asserts that feelings of hunger emanate from low proportions of glucose being used by the neurons (Morrison et al., 2009). As a consequence blood glucose from both arteries and veins supplying blood to the brain and subsequently to the neurons is also low reducing activity in the region. The induced feeling to the individual is therefore that of a need to consume food to increase the glucose levels in the blood.
These results are largely consistent with previous effects of serotonergic anxiolytics and suggest that leptin may have some serotonergic anxiolytic action coupled with serotonergic release of corticosterone.
In the FI60 task 0.5mg/kg of leptin produced an anxiolytic-like effect similar to that shown by the active control chlordiazepoxide and the 1.0mg/kg dose produced an overall depression in responding similar to buspirone and fluoxetine.
Two animals were then administered leptin at doses 0mg/kg (control), 0.5mg/kg, and 1mg/kg (i.p.) and produced a 30 – 90 minute dose-dependent increase in the slope of the stimulation/frequency function of but did not change overall frequency.
Perhaps one of the most comprehensive hypotheses is that dealing with dealing with the lipostatic conditions of the hypothalamus. This theory is based on the hormone leptin, which is an ob gene product, as being a major determinant of food intake as it acts on the hypothalamus and inhibits the intake of food and consequently increasing energy output (Ling, 2004). The adipose tissue is credited as initiating this process by its production of a signal that is relayed through the blood and other body fluids to the hypothalamus depending on the amount of fats registered by this region.
We predicted that our hippocampal RSA test of anxiety would show a food-modulated circadian pattern of oscillation; and that leptin would have an anxiolytic-like effect on both reticular-stimulated hippocampal RSA and behaviour in the FI60.
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Banks, W.A., Coon, A.B., Robinson, S.M., et. al., 2004. Triglycerides induce leptin resistance at the blood-brain barrier. Diabetes, 53(5), 1253-1260.
From an overall analysis of the common ground achieved from the diverse research initiatives, the control of food intake can be considered as being determined by neural circuits in the hypothalamus (Davies, Fitzgerald & Mousouli, 2007). The insights into the networks of the various neurons and actual intermediaries in the process have also increased over the past decades. Research has extended past food intake into the effect that the hypothalamus has on body weight and even severe cases such as an individual being overweight. By analyzing the potential links between food intake and hormones such as leptin, scientists have been able to formulate possible associations between the hypothalamus and obesity.