During the digestive phase, lipoproteins play a crucial role in energy metabolism. Dietary fats, including glucose and fructose from carbohydrates, are transported through adipose capillaries. Lipoprotein lipase (LPL) facilitates the extraction of free fatty acids (FFAs) from chylomicrons within adipose tissue capillary beds, while chylomicron remnants are eliminated by the liver. Insulin promotes this process by stimulating the activation of FFAs and inhibiting hormone-sensitive lipase (HSL), preventing the release of FFAs. Additionally, insulin stimulates glycolysis in adipocytes, generating glycerol-3-phosphate (G3P) for the reesterification of FFAs into triglycerides (TGs).

In the fasting phase, glucagon and catecholamines activate HSL, resulting in the release of FFAs and glycerol from stored TGs. Without the presence of insulin, these products of lipolysis are exported into the bloodstream. 

Protein metabolism is also influenced by hormonal regulation. Insulin promotes protein synthesis by facilitating amino acid uptake and mRNA translation while inhibiting proteolysis. During the digestive phase, insulin promotes protein synthesis and attenuates the activity of urea cycle enzymes in the liver. Conversely, glucagon and catecholamines activate proteosomal degradation of proteins and the release of amino acids during the fasting phase.

Lipoproteins play a vital role in transporting lipids through the bloodstream. Free fatty acids primarily circulate bound to albumin, while other hydrophobic molecules such as triglycerides, free cholesterol, cholesterol esters, phospholipids, and lipid-soluble vitamins are transported within lipid-protein complexes called lipoproteins. These complexes consist of a mix of the aforementioned lipids and specific apoproteins. The TG-rich lipoproteins, known as chylomicrons and very-low-density lipoproteins (VLDL), deliver FFAs (in the form of TG) to skeletal and cardiac muscle for energy and to adipocytes for storage. On the other hand, cholesterol-rich lipoproteins such as low-density lipoprotein (LDL) and high-density lipoprotein (HDL) transport cholesterol to proliferating cells, steroidogenic cells, and hepatocytes responsible for bile production. HDL also removes excess cholesterol from peripheral tissues, including cholesterol from macrophage-engulfed dead cells. Additionally, there are remnants of lipoproteins that undergo partial lipid digestion and are subsequently cleared from the bloodstream by the liver.

During the digestive phase, chylomicrons and chylomicron remnants are formed as triglycerides from a meal are enzymatically digested into free fatty acids (FFAs) and 2-monoglycerides within the intestinal lumen.
714 SECTION8Berne & Levy Physiology •Fig. 39.16 Roleoflipoproteinsinenergymetabolism.A,Digestivephase.B,Fastingphase.Dietary fats Adipose capillaries Dietary sugar & carbs Glucose fructose CM Adipose capillaries LPL CR Cardiac muscle capillaries LPL FFAs FFAs A B FFAs FFAs Cardiac & skel muscle capillaries LPL Cardiac & skeletal muscle Steroidogenic cells Growing cells FFAs TG TG Adipocyte Adipocyte TG Liver VLDL Glucose fructose Cardiac muscle ATP Skeletal muscle ATP KBs TG Liver ATP CHOL ATP IDL LDL IDL within adipocytes and its migration to the apical side of endothelia in adipose capillaries (reaction 1D). This action of insulin allows LPL to extract FFAs from chylomicrons within adipose tissue capillary beds (reaction 2D). The chylomicron remnants (discussed later) are removed by the liver. Insulin also stimulates activation of imported FFAs by their conversion to fatty acyl CoAs (reaction 3D). Insulin stimulates glycolysis in adipocytes, which generates the G3P required for reesterification of FFAs into TGs (reaction 4D). Insulin directly inhibits hormone-sensitive lipase (HSL; reaction 5D), thereby promoting storage of FFAs as opposed to their release. During the fasting phase, glucagon and catecholamines phosphorylate and activate HSL (reaction 1F), thereby promoting release of FFAs and glycerol from stored TG (reaction 2F). In the absence of insulin these two products of lipolysis are exported into the blood.
Protein Metabolism in All Hormone Target Cells: Digestive vs. Fasting Phases
Insulin promotes protein synthesis in muscle and adipose tissue by stimulating AA uptake and mRNA translation. Insulin also inhibits proteolysis. Although the liver uses AAs for ATP synthesis, insulin also promotes synthesis of proteins during the digestive phase and attenuates the activity of urea cycle enzymes in the liver. Glucagon and catecholamines activate proteosomal degradation of proteins and release of AAs during the fasting phase.
Metabolic Roles of Lipoproteins: Digestive vs. Fasting Phases
This section deals with lipoproteins in some detail. For more details, consult a biochemistry textbook.
FFAs circulate in the blood primarily bound to albumin. However, TG, free cholesterol, cholesterol esters, phospholipids and some lipid-soluble vitamins, all of which are hydrophobic and would partition into the membranes of endothelial cells instead of circulating, are transported through blood within lipid aggregations (i.e., a mix of the above) bound by specific apoproteins. These lipid-protein complexes are referred to as lipoproteins. The TG-rich lipoproteins are chylomicrons and VLDL and primarily function to deliver FFAs (as TG) to skeletal and cardiac muscle for energy and to adipocytes for storage. The cholesterol-rich lipoproteins include low-density lipoprotein (LDL) and high-density lipoprotein (HDL), which deliver cholesterol to proliferating cells, steroidogenic cells, and bile-producing hepatocytes. HDL also removes excess cholesterol (i.e., from macrophage-engulfed dead cells) from the periphery. There are also “remnants” of lipoproteins that have their lipid cargo partially digested and then cleared from the circulation by the liver.
Digestive Phase: Chylomicrons and Chylomicron Remnants
TGs in a meal are enzymatically digested to FFAs and 2-monoglycerides within the lumen of the intestine.