Just read an intriguing article entitled Cell-Specific Competition for Calories” Drives Asymmetric Nutrient-Energy Partitioning, Obesity, and Metabolic Diseases in Human and Non-human Animals. It is insightful.
Years ago I did lots of animal surgery. I noted, especially in rats which accumulate fat pads as the top of their front shoulders, that these adipose beds were heavily vascularized. Once fat cells are created (hyperplasia), they persist as the most accessible ‘sink’ for postprandial glucose, fatty acids & amino acid excursions. With this metabolic ‘sinkhole’ for glucose, fatty acids, and de-amidated amino acids to ‘fall into’ postprandially, it is easy to see why weight loss and subsequent weight maintenance is so difficult.
Prior to adipocyte hyperplasia in an animal or human, caloric nutrients (glucose, fat, amino acids) have to circulate in the blood until actively transported into muscle cells, liver cells, immune cells, brain cells, etc. Once adipocytes are created, there is a new, ‘easy’ path to remove these metabolites from the blood with the benefit of longterm energy conservation. And after nutrients leave the bloodstream, humans and animals want to eat (manage managing hunger/appetite) or respond to signals to release these same energy sources into the blood to fuel our activities and basic cellular functions.
Thank you to these authors for making this ‘regulatory’ story so much clearer.