We have considered homeostatic mechanisms in various contexts. What is a homeostatic mechanism? Homeostatic mechanisms maintains stable conditions with respect to any given physiological parameter. Consider homeostasis of thoracic temperature during flight; of hemolymph energy metabolite concentrations; of water balance in terrestrial insects; of osmotic balance; of symbiotic organisms. Two aspects of physiology are implied in discussions of homeostatic mechanisms: first, organisms can register changes in an homeostatic parameter, and second, features of the parameter can be adjusted. In homeostasis of thoracic temperature, it is clear that thoracic temperature is monitored during flight (even if we do not understand the measuring system), and it is clear hemolymph circulation patterns are adjusted in response to changes in thoracic temperature. I introduce a discussion of the insect fat body in terms of homeostasis for a couple of reasons. First, fat body is involved in many homeostatic mechanisms; second, I want to emphasize the point that fat body is an active center of metabolic activity.

In most insects the fat body serves as a storage depot for food reserves, and sometimes for storage excretion. Lipid reserves are often accumulated in massive quantities in this organ, so that it looks like a body, or organ, of fat. The term fat body was coined during early days of studying insect morphology, and it derives from the fatty appearance of the tissue. This term is deeply entrenched in the literature of our field, so much so that it would be a futile exercise to try working toward a more descriptive expression for this organ. The alternative is to expand our conception of what the term fat body represents.

In addition to its important roles as a storage depot, the fat body of insects functions as a key center of metabolism and biochemistry. As a metabolic and biochemical center, the biological significance of fat body is its ability to maintain a balance between resources and requirements during the many phases of an insect's life. On one side of the balance, during times of feeding fat bodies biosynthesize and accumulate not only lipid reserves, but also carbohydrates, amino acids, proteins and other metabolites. On the other side, fat bodies respond to physiological and biochemical needs in a number of ways, including very high rates of protein biosynthesis, formation and release of trehalose, release of lipids, detoxification of nitrogenous waste products, and biosynthesis of hormones. Many of the responses to physiological needs occur on a relatively large scale, and they can have substantial impact on insect biology. Very often fat body metabolic functions are regulated by various endocrinological mechanisms.


Structures of fat bodies


The morphology of fat bodies varies considerably in various insect groups. In many species it is a loose aggregation of cells that may be unevenly distributed among all body segments, including the brain case. Fat body cells often surround the major organ systems in insects, including reproductive tissues, alimentary canals, thoracic muscles, and elements of central nervous systems. This close association of fat body cells and other tissues may facilitate exchanges of macromolecules. Fat bodies may also protect organs from physical damage by providing packing. In other species fat bodies are compact cell masses invested in a membranous covering such that they easily can be removed from the insect intact.

Structures of fat bodies may vary according to life stage, sex and reproductive status. Fat bodies can have different functions between sexes, and functions also can differ among life stages. In some species they undergo histological breakdown and reformation during papal stages, though in most species they do not appear to do so.

Fat bodies of all insects are in intimate contact with circulating hemolymph, which is consistent with movements of molecules between the two compartments. The vast majority of the cells in fat bodies are called trophocytes, and it is in these cells that most fat body functions are carried out. Trophocytes are very similar to some hemocytes; the two cell types may be quite closely related. In the homopteran Aleyrodes, for example, fat body cells float individually in hemolymph and can not be clearly distinguished from hemocytes.

Other fat body cell types include urate cells. These cells are associated with storage excretion, in which uric acid crystals are accumulated rather than excreted. Fat bodies of most insect species do not include urate cells. For the sake of complexity, uric acid is stored in trophocytes of some species. Fat bodies of many species also contain mycetocytes, which are involved in housing symbiotic micro-organisms. Many of these symbiants play crucial roles in insect nutrition by providing certain vitamins and other essential nutrients to insects that are not able to acquire these nutrients in the diet.


Protein biosynthesis in fat body


Many of the proteins that are crucial in the lives of insects are biosynthesized in fat bodies. Protein synthesis is often under control of juvenile hormone (JH). One of the most well-studied examples of endocrine regulated protein synthesis in fat bodies is the formation of vitellogenins by adult females. Vitellogenins are the yolk proteins that are accumulated during egg maturation. Fat bodies biosynthesize many other proteins as well, including virtually all of the major proteins found in the hemolymph of larval insects. There are also many examples of specialized proteins in insects. Larvae of the midge Chironomus biosynthesize hemoglobins, heme-containing proteins important in storage of oxygen. Hemoglobins can make up more than 80% of the hemolymph proteins in these larvae. The lipoproteins that function in hemolymph transport of diacylglycerol are synthesized in fat bodies. There are many other examples, all bearing on the point that protein synthesis in fat bodies is a central issue in insect biology.

We review the biochemistry of protein synthesis by way of appreciating the importance of this topic. First we recall the expression originally put forth by Francis Crick, and later articulated by Charlie Brown as the central dogma of molecular biology: DNA MAKES RNA MAKES PROTEIN. As an aside, a group of my biochemical colleagues at the University of Nevada, Reno and myself once entered a biochemical T-shirt logo contest. We added the expression makes lipids to the expression of the central dogma of molecular biology. We did not win. This figure shows that genes are transcribed from DNA to RNA within a cell nucleus.

The transcription process produces a special form of RNA called messenger RNA, or mRNA. Messengers go places, and in this case mRNA makes its way from the nucleus to the cytosol where it joins with ribosomes, modeled in the figure. We want to see that the mRNA is joined with two ribosomal subunits, a small and a large subunit. The next figure shows this is a little more detail. The flow of information is from the nucleus to the cytosol. This is followed by a series of steps that include translation of the genetic information borne on the mRNA strand into a polypeptide chain, or string of amino acids. The key here is that each of the amino acids can be attached to a specific RNA molecule known as transfer RNA, or tRNA. One portion of tRNA molecules feature an anticodon that matches up to codons on the mRNA strand. Ribosomes have sites for two tRNA molecules, one called a peptidyl site and the other called an aminoacyl site. While two tRNA molecules are juxtaposed within the ribosome a peptide bond is formed between the amino acids attached to each tRNA. At this point the tRNA molecule in the peptidyl site is released and the ribosome scoots one step along the mRNA strand, thereby shifting the tRNA molecule in the aminoacyl site to the peptidyl site and opening a space for a new tRNA molecule. The cycle goes on with addition of the new tRNA molecule, formation of another peptide bond, release of a free tRNA molecule and another ribosomal shift. A copy of the universal genetic code is appended to the end of this column. Please note, for example, that the AGG in the mRNA strand shown above specifies the amino acid arginine.

Protein synthesis begins with transcription of a DNA strand within a cell nucleus. JH expresses its effects on protein synthesis within fat body cells by interacting with DNA. JH receptor proteins are found within the cytosol of cells. JH forms a complex with its specific receptor, then the hormone-receptor complex moves into the nucleus. It is the JH-receptor complex that interacts with DNA.


Carbohydrate metabolism in fat body


The natural foods of many insects include substantial amounts of carbohydrates, or sugars, either in the form of simple sugars or as polymers. Following absorption across midgut epithelium, sugars are removed from circulating hemolymph into fat bodies. Sugars are assembled into large macromolecules of glycogen and stored within fat bodies (try to imagine a discussion on the physiology of the sugar body). The polymerization of simple sugars into glycogen is called glycogen synthesis, and is carried out enzymatically by glycogen synthetase. It has been suggested that glycogen synthetase may be under control of a sort of hypoglycemic hormone. There are a number of lines of evidence for factors that reduce hemolymph sugar levels, but the specific points of control remain unknown.

But there is also evidence for endocrine regulation of carbohydrate mobilization. Various names have been applied to hormones that increase hemolymph sugar levels, including hypertrehalosemic factor and glucogon-like hormone. Most recently people have been using the term trehalogon by analogy to the mammalian hormone GLUCOGON. I think such words give insect endocrinologists a bad name, but there you have it. Trehalogon is thought to stimulate fat bodies to release trehalose into circulating hemolymph.

Releasing trehalose into hemolymph is a multi-step process that begins with hydrolysis of individual glucose residues from glycogen. This next figure shows this is under control of the enzyme phosphorylase, so named because phosphorus is involved in the hydrolysis. This enzyme yields molecules of glucose-1-phosphate, which are taken into two pathways, one is a mutase step to glucose-6-phosphate and the other is a phosphorylase step to uridine diphosphoglucose. These two glucose derivatives are combined into trehalose-6-phosphate by trehalose-6-phosphate synthetase. A phosphatase step yields the free trehalose molecule. Hence, trehalose synthesis requires hydrolysis, derivatization and assembly of two glucose residues.

Trehalose synthesis is regulated by controlling the activity of phosphorylase, the enzyme at the beginning of the pathway. There appears to be two forms of phosphorylase, phosphorylase a, the active form and phosphorylase b, the inactive form. Both of these forms exist in fat bodies, and the specific ratio of one form to the other depends upon the physiological requirements of the whole organism. Physiological requirements are expressed by circulating titres of trehalogon, the hormone active in mobilizing fat body trehalose. A final point is a reminder that the figure as shown here is taken from a recent compendium on the endocrinology of insects. It contains a slight error, shown in the phosphorylase step. This step requires the input of inorganic phosphorus, just the opposite of what is shown.


Metabolism of lipids in fat body


We have seen that lipid reserves are stored in fat bodies as triacylglycerol. Triacylglycerol is synthesized in fat body from excess sugar and from the carbon skeletons of certain amino acids by way of the ubiquitous enzyme system fatty acid synthetase. Newly formed fatty acids are linked to glycerol backbones by acyltransferases.

Lipid is released from fat body in the form of 1,2-diacylglycerol (DAG), rather than as 1,3-diacylglycerol or a mixture of 1,2-DAG and 1,3-DAG. 1,2-DAG may be formed directly by a lipase specific to the 3-position fatty acid, or it may be formed by breakdown to 2-monoacylglycerol followed by stereospecific reacylation to 1,2-DAG. Release of 1,2-DAG is stimulated by adipokinetic hormone, but the particular enzyme target is not yet known.


Uric acid synthesis and other detoxification reactions


The details of uric acid synthesis will be covered in the section on nitrogen metabolism and excretion. The point to emphasize here is that the fat body is the central organ of nitrogen metabolism. The storage of uric acid in urate cells and in trophocytes by some insects has been covered.

One of the great problems in crop protection by application of chemical pesticides is the natural resistance to these poisons that insects rapidly develop. Two broad mechanisms of resistance are enzymic breakdown steps, one by esterase and another by mixed-function oxidases. Under these systems, the pesticide molecules are simply metabolized into harmless forms before they can carry out their damaging effects. Most of these detoxification enzymes are formed in fat bodies and function in circulating hemolymph as well as in fat body cells.


Biosynthesis of amino acids in fat body


The non-essential amino acids can be formed using carbons from various intermediates in carbohydrate metabolism coupled with transaminations from preexisting amino acids. The fat body is the major site of amino acid synthesis.


At least one hormone is synthesized in fat body


Most homeostatic hormones, such as diuretic hormone, adipokinetic hormone and trehalogon are released from elements of corpus cardiacum or from elements of neurosecretory cells. There is an example of a hormone that is produced and released from the fat body. About 40 hours after taking a blood meal, adult female mosquitoes produce what is tentatively called host-seeking behavior inhibitory factor. This factor is a small peptide, and is produced in fat body and released into circulating hemolymph. The exact site of action remains to be found, but one physiological effect is to switch off specific lactic acid receptors located in antennae. Fat bodies need to be physiologically prepared to synthesize the factor. Another hormone appears to be required because females that have been ovariectomized within three hours after a blood meal do not elaborate the factor.

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