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Chitin (part 1):
Chitin is the exoskeleton of insects/larvae/crustaceans. It is carbon molecules very similar to plant cellulose, except where cellulose has a hydroxyl group in the carbon array chitin has an acetamido group (an acetyl & amino.
The value added product made from chitin is a polymer called chitosan. The characteristics (solubility) of a chitosan end product is a function of how it was processed.
There are factors like the ratio of chitin to alkalai processor (sodium hydroxide, NaOH), % alkalai used, temperature (& to a lesser extent time), the source of the chitin substratate that undergoes cleaving it's acetyl (de-acetylation), resultant particle size & any further treatments to the extracted chitin (chitin free from protein) that is isolated from the crude substrate (exoskeleton).
Chitosan's original substrate chitin, conversion methodology & end product elaboration results in different amino & acetamido group sequences. The gained NH2 amino/acetamido groups permit chitosan to have biological functions.
Because processing replaces the original chitin's ...C-CH3 acetyl groups a higher degree of de-acetylation in end product chitosan is usually more desirable. Quality chitosan will have a low % of ash if the processor removed most of the residual protein associated with the original chitin carbon backbone; this improve the solubility of chitosan.
Chitosan has a + cationic protonation feature, but it doesn't just have the ability to link to negative charges. It's amino NH3+ groups allow it to aggregate with other + polyanionic (multiple + charges) compounds & chelate them; chitosan has the ability to accept + cations.
Chitosan is a weak base & pH drops protonate (protons come into play) it's + charged aminos into cationic poly-electrolytes. This causes the chitosan plolymer to swell due to electro-static repulsion of the polymer's internal groups having the same charge, that are then soluble.
At over 6pH the aminos are de-protonated; which means that charge is lost keeping chitosan insoluble. At over 6.5 pH the simple ("acid soluble") type of chitosan polymers aminos have larger aggregates with some phase separation; in layman's terms it is very viscous.
In contrast, from 6.5pH down to 5.2pH the chitosan polymer's structural aggregation declines. This is due to molecular coils compacting & thus allowing freer amino groups' H (hydrogen) bondings to a neighboring O (oxygen) chain in the polymer matrix.


  • Chitin (part 2):
    Chitosan induces chitinase & chitosanase enzyme activity; while there are not just a single type of either enzyme - nor are their respective functions always the same. For example a single fungi can genetically encode anywhere from 2 - 27 different chitinase enzymes (the average for a single fungus is 15 chitinase genes) & a bacteria will have 2 - 4 different chitinase enzymes.
    Micro-organisms have some negatively charged macro-molecules on their cell surface which chitosan's numerous + cation sites can latch onto. The chitosan polymer gets acted on by chitinase & chitosanase spinning off hydro-lysis (splits apart)byproduct that a cell responds to.
    Classification of chitinase enzymes is convoluted. I will oversimplify the distinctions.
    There are fungal & bacterial endo-chitinase (inside) with chitin binding grooves that are like tunnels & deep tunnels. In these tunnels the enzyme can degrade chitin anywhere on the chitin polymer chain to yield byproducts of random lengths.
    Then there are the exo-chitinase (outside) with chitin binding grooves that are open & not deep grooves. These only can work at a non-reducing end chain of the chitin polymer to yield N-acetyl-glucosamine (GlcNAc)2.
    Both kinds of chitinase (endo & exo) can work so that: after perfoming hydrolysis the enzyme moves off the chitin polymer & thus get short (2-8 mer) byproducts. Or, some after performing hydrolysis the enzyme passes the chitin chain that it is on for yet another cleaving operation & this time get long (6-8 mer) byproducts.
    And to complicate the classification there are 3 subgroups of all the chitinase enzymes. The size of one subgroup is 40-50 kilo Daltons, another 30-90 kD & also 140-170 kD with their attendant properties. Each chitinase can present carbohydrate binding molecules specialized for chitin & C (carbon) molecular patterns.
    Chitinase enzymes are classified as belonging to the glycoside hydrolase enzyme family 18 & family 19. They drive hydrolysis of beta-14 links in chitin & chito-oligomers (accretions) to spin off short chain chito-oligomers. Those that pertain to family 18 or 19 have different 3 dimensional configurations, different catalytic workings & different anomeric byproducts.
    Chitin, & the chitosan made from it, can be seen arrayed in parallel chains of chitin (called beta-chitin) or arrayed with the chitin chains anti-parallel (called alpha-chitin); there is a variant of alpha-chitin called gamma-chitin.
    Making chitosan properly from alpha-chitin converts it to a parallel beta-chitin chained polymer (desirable). The alpha-chitin chains are all held apart at 0.47 nm & their sheeting arrangement make it insoluble. In contrast beta-chitin's sheets of chains have no appreciable distance & thus is more capable of intra-crystaline swelling (solubility).
    Insect chitin contents are: butterfly = 64%, sillkworm = 44%, waxworm = 33%, beetle = 27-35%, cockroach = 18-20% & diptera fly = 54% (fly chrysalis can be 80% chitin) s.
    But original substrate 's chitin content is not an indicator of how much chitosan produced from that substrate. For example lobsters's 47% chitin only yield 20% chitosan & to make 1 Kg of chitosan that is 70% de-acetlyated from shrimp shell chitin uses ~2 Kg NaOH plus ~ 6Kg HCl for processing. Most commercial chitosan is made from 64-69% chitin rich crab shell (king crab is 35% & blue crab only 14% chitin).
    Some links:
    *(2013) "Physiochemical properties & antioxidant activity of chitosan from the blowfly Chrysomya megacephala larvae"
    *(2011) "Preparation and characterization of Food-grade chitosan from fly larvae"
    full free text =
    *(2012) "Extraction and characterization of chitin from the beetle Holotrichia parallela Motschulsky " (in journal "Molecules 2012,17,4604-4611)=

  • Chitin (part 3):
    Some chitinase enzymes present domains of serine/threonine that have no fixed structure. This gives them unusual potential to interact with chitin they encounter.
    Chitinase with more than 1 domain that can bind to chitin are capable of binding to select carbohydrate on the cell wall of pathogenic gram negative bacteria. The gram negative bacteria agglutinates due to multi-dimensional molecular changes on it's cell wall & inhibits that bacteria's ability to move/grow.
    Lectins are molecules with at least 1 chitin binding domain. But there are many types of chitinase enzymes that have more than 1 chitin binding domain.
    Pathogenic fungi defend themselves by producing what is called an avirulence protein for their own chitin walls. It is a tactic to make it harder for the funal host's chitinase enzymes to access the pathogens cell wall to degrade it.
    Time and concentration of chitosan vary in how it alters the length and area of fungal condia that become altered. When chitosan upregulates the local amount of beta-1-3-glucanase enzyme & at the same time induces chitinase enzymatic activity this thins the growing end points of fungal hyphae. The fungal mycelium forms aberrantly &,
    depending on types, sometimes the mycelium swell or other times the mycellium lose volume - but either way fungal nutrition is equally impaired.
    Chitosan is also finding uses for medicinal plants; one carefully analyzed is the root of Garcinia (Hypericum perforatum) production of xanthone, which treats Candida (fungal) & dermatophytes. A week after chitosan application there were more bio-active compounds with high anti-fungal values (MIC ug/ml) than the control.
    Chitosan that requires "acid" solubility can be further processed to make O-carboxylated chitosan, oligo-chitosan & pharmaceutical grade chitosan. In part it has to do with what molecular weight is suitable for what application.
    Carboxymethyl chitosn is chitosan end processed with mono-chloro-acetate in NaOH to derive carboxy-methyls. The temperature of carboxylation determines if get an N or O-(ideqal) or N- (undesirable) carboxymethylation. O- link makes for more affinity for outside ions because the hydrophobic methyl groups have broken hydrogen bond & then the carboxyl groups maximize solubility.
    A hemostatic surgical sponge that can be absorbed has been elaborated with chitosan from fly larvae chitin. Elsewhere, the chitosan sponge with platelet derived growth factors proved useful in bone regeneration; there are several variations of molecules that have been tested in the chitosan sponge.
  • I've actually been reading about chitosan recently; it would be interesting to incorporate chitosan into the economic model for a farm. It could certainly help offset production costs. In species that leave their shed exoskeleton intact after molting, it might be an easily harvestable byproduct that doesn't require any separation.
  • I am not a scientist, so most of the details were over my head. My basic understanding of this is there are products that can be made from the exoskeletons of insects. In laymen's terms, without explaining the process at the molecular level, what products might be made from chitosan?

    Sorry for my lack of academic understanding. I ask because I thought others who do not have a background in biology might stumble upon this and be interested in this potential byproduct.

  • Hi William, For example chitosan is used as something to build bone around ("scaffolds"); as per (2004) "Chitosan–alginate hybrid scaffolds for bone tissue engineering" ....or, as something to coat a probiotic for better delivery ("viability"); as per (2014) "Enhanced viability of probiotic Saccharomyces boulardii encapsulated by layer-by-layer approach in pH responsive chitosan–dextran sulfate polyelectrolytes"....And many other uses if you have a particular interest to ask about....I think a refined grade akin to a "pharmeceutical" purity chitosan is sold as a dietary supplement for weight loss; but can not vouch it's effectiveness...I use one of the several lesser processed types of chitosan that dissolves in water for agricultural applications. It can be used as a seed pre-planting treatment for seedling emergence & root development, among various other things.... For your micro-greens I do not think it worth pre-treating the seeds with chitosan because those greens are harvested before any significant root branching is needed. Now, in the case of very old seeds with poor germination rates then a chitosan pre-treatment has been experimented with & reported to be helpful for increasing germination.

  • William, While I have scientific background, the discussion here is beyond me as well. It does seem like collecting the exoskeleton during the production of commercial quantities of insects would be easy to do. In my home-based mealworm colony, the exoskeletons accumulate on the surface of the substrate. I typically take my containers out doors and let the wind ( or my breath) blow that layer away. I've noticed that the exoskeleton seems to be attracted to some electrostatic charge on the plastic drawers, also. So, there should be an easy method of collecting this byproduct, if it is valuable to anyone. We'd need to investigate the cost of collection compared to the economic return, of course. But, it would be ideal to find a way to reuse or recycle a significant waste product.


  • From a business standpoint, I would expect that shrimp shells would be a very low cost raw material for further process chitin products. Compost would probably be the best home for small scale production.

  • Chitin cross-post from elsewhere in the Forum: Chitin can be a useful dietary ingredient in cricket feed; which also makes sense since we know crickets do cannibalize other crickets.

    However, feeding chitin to crickets in not a simple linear function; it depends on other components in the feed formulation. What needs to be distinguished is whether the cricket diet is low in cellulose/roughage or high in cellulosee/roughage determines how useful chitin in their feed turns out.

    Basically, if the cricket diet is going to be high in roughage & very low (to no) in carbohyrates adding chitin will result in a inferior rate of growth. Thus if a commercial operations readily available feed already has a lot of roughage/cellulose you would not want to supplement that with very much chitin (ie: keep cellulose + chitin total to a maximum of 48% roughage components in total feed; as per 2nd paragraph below).

    On the other hand, a cricket diet that is by necessity low in roughage by choice (ie: suits the project's economic plan) or circumstance (unreliable raw material availability) can feed chitin for improved weight gain. In practical terms this means a low roughage/cellulose diet supplemented with 30% chitin will let young crickets gain weight. See Table 3 in link below.

    Cited study also concludes that crickets need 25-48% roughage + 6-29% "sugar" for an ideal artificial diet. A intriguing technical discovery is that the type of plant sugar also impacts early (study did not continue past 3 weeks) cricket growth.

    Ribose, xylose, arabinose, sorbose & galactose derived plant "sugars" seem to be inhibitory to 3 week old cricket growth. Carbohydrate "sugars" stimulating growth for the same age crickets are mannose, cellopbiose , glucose, fructose, mannitol, maltose , glycogen, trehalose & sucrose. See Table 4 in link below.

    Now, trehalose is the "sugar" found in insects & in a decent (high) roughage diet produces 56.6 mg. crickets by age 3 weeks. What I infer from this (& cricket cannibalism) is that one could integrate a commercial cricket rearing venture with a lower cost insect rearing program (ex: fly larvae?) which can be ground up (the lower cost insect) for feeding to the crickets.

    Consider the labor cost of handling the cricket roughage stream & outlay for the raw material itself. Compare that with having a less costly waste reared insect (these could be shipped in cheaply) that then can grind up for it's trehalose content, the chitin & then supplement with roughage if that is most cost effective (I am not sure it is, commercial operations need to develop their own proprietary protocols to be competitive with innovations).

    Data from : (1962)"Carbohydrate and Roughage Requirement of the Cricket, Acheta domesticus", by Neville & Lucky of Department of Biochemistry, University of Missouri, School of Medicine, published in the Journal of Nutrition; free full text =

  • Yes but how do we make Viktor Grebennikov's flying machine? All joking aside i read somewhere that humans Cannot digest chitin and that it may damage your digestive system. Is there real danger from this or not really? Is there a better thread for this?

  • edited December 2015

    Bugbug, in 1950'ish Bodenheimer's Insects as Human Food he writes about how apes died from obstipation by the legs from locusts as they have sharp hooks that got stuck. They learned however from it. I don't know if chitin's poor digestion in the form of cricket meal will give problems; it might even promote digestive activity IF it acts similarly to fibers.

  • Hi Bugbug, - Humans, like other mammals, have enzymes ( "-ase" on word means enzyme) that act on chitin; humans have one kind that hydro-lyzes chitin (both colloids & oligo-mers) called chito-triosid-ase (1995 "Purification and Characterization of Human Chitotriosidase, a Novel Member of the Chitinase Family of Proteins") & a 2nd kind that acts in acid pH called acidic mammalian chitinase (AMC-ase for short) given its acidic pH optimum, was named acidic mammalian chitinase (2001" Identification of a Novel Acidic Mammalian Chitinase Distinct from Chitotriosidase"). Data on the potential digestion of chitin by the latter enzyme can be found in (2006) "Human Gastric Juice Contains Chitinase That Can Degrade Chitin" (full free Author Copy pdf is available on-line). In the 2006 research Table 2 dealing with 25 adults in Italy a range of chitin degrading was revealed among individuals with 5 subjects having 0.046 nano-mole/mL/hr. chitino-lytic ( "-lytic/-lysis" means breaks apart) activity going on, 15 subjects having some chitino-lytic activity of f 0.299 nano-mole/mL/hr. & another 5 subjects having high 6.80 nano-mole/mL/hr. chitino-lytic action.

    In regard to eating insects those 2006 authors end with the following (quote): " ... higher AMC-ase (acidic mammalian chitinase) activity in tropical human populations with a higher rate of entomophagy could represent an adaptative response to alimentary habits, conferring increased resistance against parasitic infection in these areas ..." And earlier in the report state that some individuals lack stomach located chitin degrading enzymes (quote): "... absence ... chitinase ... in ... 5–6% of healthy Caucasian individuals ... due to homozygous duplication of 24 bp in exon 10 of the CHIT gene and 35– 45% of them are heterozygotes ... difference in in healthy subjects from Africa, Sardinia and Sicily that depends on the allelic dosage in these individuals ... more abundant in African subjects of poor socioeconomic conditions ...who maintain the wild-type CHIT gene (99%), while in Western countries the wild-type CHIT gene seems to have become redundant (55–65%)...."

    The way those people who can digest some chitin (instead of merely passing it out through their intestines) works is that the enzyme 1st breaks chitin (chitino-lysis) into N-acetyl-glucosamine & then as digestion continues exposing that molecule to the natural human gastric mucus membrane (& intestine epithelium) enzyme called N-acetylglucosamine kinase there works to digest the molecular components. This is the how some people can digest chitin; but another way is if the person hosts a population of the gut bacteria that performs the chitino-lytic step (that bacteria is known as Clostridium paraputrificum).

    (2009) "Differential enzymatic activity of common haplotypic versions of the human acidic mammalian chitinase protein" published in the Journal of Biological Chemistry,284(29) found a genetic haplo-type that made for a variant (iso-form) with more chitino-lytic potential in a study of Mexicans, African-Americans & Puerto Ricans. Quote: "... pH 2.2 ... stomach acidity where AMC-ase ... highly expressed ... pH 4.6 ... lysosomes where some AMC-ase likely resides ...."; Link free full text =

  • Do you think the cricket legs pose a hazard? I wouldn't think the powder form would be bad. I wonder if it poses a risk to chickens.

  • In regard to the difference between insect frass fertilizer and common N-P-K fertilizer the folliwing may be of interest. Frass contains some shed chitin &, although not going to attack a plant, it starts up defensive pathways generating secondary metabolites in the plant.

    Plant enzymes called chitin-ase are both involved in defense & normal plant processes. In the normal root & lower leaves 1-4% of the total proteins are chitin-ase. This is in part because the phyto-hormone cytokinin holds down chitin-ase in top leaves.

    In contrast, as a flower matures the messenger RNA levels of chitin-ase rises; whereas at other developmental stage chitin-ase (as well as glucun-ase & osmotin) is greater in roots. Chitin sensing invokes defensive reactions generating hydro-lytic enzymes that make oligo-saccharide derived plant hormones that can be used for transition into flowering.

    Flowering plants that respond to changing photo-period (hours of light change) at that shift will have a decreased expression in their roots of the gene "FB" (flower bud) number 7 leading to less root chitin-ase (& beta-1-3 glucan-ase & osmotin). As the phyto-hormone cytokinin moves toward a floral bract it instigates rising activity of the gene FB numberb7-3. Downstream from cytokinin impact is the synthesis of a molecule called extensin that in concert with beta-1-3 glucan-ase enzyme gives rise to flower formation.

    Osmotin is naturally found in all plant tisdue & a bit in basal internodes. When there is any wounding of the plant, like insect herbivores might do, about 6 hours later the level of osmotin can rise around 16 times higher; but then by 24th hour osmotin level can go back to baseline amount.

    Osmotin (encoded by gene FB number 7-2) levels rise in pre-floral & floral apices; in other words osmotin rises in floral organs as they develop. This is one way plants respond to heavy insect predation by rushing to flower before they are wounded too extensively to go to seed for reproduction. [[ As explained earlier in thread chitosan is used as an agricultural application to get earlier flowering.]]

    Continues ...

  • Continuation:

    What needs to be figured in to plant dynamics is the inter-play of plant hormones. There is a segue of dominance & subsidence that occurs; this makes it hard to give linear descriptions of what are useful when. For example if spray a kind of cytokinin on a leaf the gene FB(floral bud) number 7-3 messenger RNA level will not go up, even though the same kind of cytokinin naturally sees that same messenger RNA level go up in floral bracts.

    Back to the wounding (as a proxy event for insect/plant interaction) & it's cyclic alteration of osmotin, we see various phyto-hormone reactions. Wounding leads to a plant defense pathway that produces the phyto-hormone jasmonic acid (jasmonate); rising jasmonic acid levels in turn provoke a temporary alkalinization that results in more ethylene (hormone).

    Wounds cause the release of linoleic acid that is used to make additional jasmonic acid. Once the ethylene boost occurs ion fluxes occur that make it posdible to synthesize defense proteins. The plant makes the peptide called systemin, which activates protein-ase 1& 2 enzymes to move around (trans-locate) to defend against percieved "pathogen/bug" attack.

    Some of the "pathogen" defense proteins are seen a greater number of protein-ase inhibitors (anti-feedant to bug) in the plant tissue. Others are creating more cell wall components that are suitable for cross linking; this increases lignification that makes the plant sturdier.

    Plants synthesize secondary metabolite compounds with the impetus from the confluence of ethylene & another plant hormone called abscisic acid - with only trace amounts of gibberellin phyto-hormone, since excess gibberellin degrades ethylene & absisic acid. Chitosan/chitin provokes plant to make more absisic acid & then that hormone out-competes gibberellin for a binding site.

    Phenolics are secondary metabolic molecules that increase in the plant from exposure to chitin/chitosan; these are the plant's 1st response to attack (pathogen or bug munching). Frass, due to it's chitin rather than N-P-K content, can make more compounds in the plant that humans find interesting.

    Again, there is an issue with interplay rather than creating a constant state. Unconstrained ethylene usually holds down secondary metabolites, however it does generate secondary metabolite indoles; these then increase terpene synthesis.

    Wounding, & by extension reaction to chitin/chitosan, down shifts the level of an auxin phtyo-hormone degrading hormone (IAA oxid-ase) leading to more auxin being around. Ethylene phyto-hormone elicits more plant made kaempferol (flavenoid) that in turn lowers IAA oxid-ase stopping hasty natural auxin (IAA) break down. In plant cells that are mature there is less auxin because those cells normally have high base-line levels of IAA oxid-ase.

    The commercial use of foliar chitosan spray is never constant because elevating ethylene inhibits shoot initiation for about 5 days; yet after that delay the impact of ethylene is more primordia ( incipient point of growth) forming. On roots the initial impact of ethylene in the 1st days is to reduced roots forming, then later increases root forming. Ethylene affects the tran-scription & localization of auxin hormone shuttlers (PIN) during developmental phases.

    Continues ...

  • Continuation...

    So chitin/chitosan fosters changes when it instigates jasmonic acid production; which occurs via the lip-oxygen-ase pathway synthesis of oxy-lipins (jasmonic acid). After this is converted into methyl jasmonate form & that then boosts ethylene levels.

    Dividing plant cells experience rising ethylene at the rate if about 1.2 micro Mole per hour until peaking when the cell hits what is classified as the stationary phase. Free auxin (IAA) in plant tissue cells rules the rate that ethylene is produced.

    Looking at root benefits from moderate chitin/chitosan challenge we find that ethylene's hormonal action on roots is modulated by the localization of auxin hormone. Auxin is a type of phenol which when ethylene levels rises is transported about.

    Ethylene has more notable impact on the initial formation of lateral roots, than primary roots because it limits elongation of lateral roots. Under high ethylene a gene produces more of the enzyme amino- tranfer-ase; the downstream result is keeping more auxin in a root stem (meri-stem) cells' meri-stematic sector, which does not have the same functionality as the root elongation zone sector.

    However, during the formation of a lateral root that has already begun to initiate primordia of a lateral root the combined synergy of extra ethylene and more auxin instigates more primary root cells (peri-cycle cells) to form in that elongating root. Those extra peri-cycle cells have the potential to generate new stem cell (meri-stem cells) that can become more lateral roots.

    Thus, cyclic decline in root ethylene removes inhibition of growth on lateral roots. In order for root hairs to form both ethylene & auxin levels must segue lower.

    Continues ...

  • Continuation:

    This may be a junction to explain how phyto-hormone auxin relates to jasmonic acid which chitin/chitosan instigates, since these 2 hormones toggle each others' transient balance. Basically, when jasmonic acid signaling is high there is altered auxin hormone dynamics.

    Methyl jasmonate is inhibitory to the growth of primary roots, yet induces lateral roots to grow. In the case of lateral roots jasmonic acid hormone causes local auxin synthesis, which lets that hormone (auxin) level become elevated at the region of a root basal stem cell (meri-stem).

    In the other paradigm, of primary roots growing, jasmonic acid can bind to root promoters integral to keeping that stem cell niche. The kind of auxin gradient there is reduced by jasmonic acid, which acts to knock down the level of one variety of auxin shuttler (PIN).

    In other words, the overall jasmonic acid effect is to increase auxin in the root basal meri-stem in such a way that increased root laterals form, but less primary roots. Sustaining the auxin gradient in primary roots is partly due to how jasmonic acid can for a complex with tryptophan amino acids &, since tryptophan is a used to make auxin this can alter the ratio there of auxin to jasmonic acid.

    For comparison, pathogenic fungi chitin elicits alot of jasmonic acid resulting in more auxin being where not suitable & compounds the problem by stalling auxin transport to clear impacted plant cells. Too much auxin in the root elongation zone inhibits those root cells.

    Whereas, beneficial symbiotic fungi (classed as ecto-mycorrhizal & arbuscular) stimulate lateral roots. The fungal chitin leads to increased local auxin in root peri-cycle cells, which causes more initiation of lateral roots.

    The reason the roots are not impacted long term by chitin/chitosan is because jasmonic acid production is also instigating ethylene production. Ethylene, once cycles along, increases the amount of auxin made & boosts auxin transport to root's elongation zone so the level of auxin goes up there. There are changes to assorted dynamics involved in auxin transport instigated by ethylene.

    In terms of how muchg chitosan is beneficial one must consider the plant's developmental stage. For initial root growth 0.01% generic chitosan will increase rootlet lenghts & 0.05% generic chitosan may be too much causing less rootlet length. When above ground growth is targeted 0.1% generic chitosan will produce more secondary metabolites (remember auxin is a phenol) leading to more shoot growth.

    I have no formula to inter-convert generic chitosan ( agricultural grade, not pharmaceutical quality) to chitin content of any particular variety of insect's frass.

  • This is far too complicated for me to understand. I wonder if Chitin from Cricket is different from shrimps' as shrimp shells can be acquired at very low cost? Is there an effective way to get chitin out of the cricket flour?

  • Hi sinadang, - Insect chitin made into chitosan is "better" than shellfish chitin made into chitosan. Among different insects there are some whose chitin made into chitosan is "better" than others' chitosan product; this grading of "better" is also found in chitosan made from different shellfishs' chitin.

    The commercial production is greatest (& probably most economical) from crab chitin made into chitosan. In part because of the size of their exoskeleton & there are many shelled generating their chitin containing shell in large factories for marketing to humans.

    I don't make cricket flour & can not speak from experience on it's consistency. In theory if you grind it fine & them sift it through an "x" (to be determibed) micron pore cloth the chitin polymer shards will collect in mesh, as the non-polymer components (ex: protein) that grind finer pass through.

    I do briefly boil fresh yellow mealworm larvae, ferment them in whey, store refrigersted, before consumption wash them, process to a slurry in a blender & filter that through cloth (old tee shirt weave). The chitin collects in the pressed cloth (I don't eat that because don't like the mouth feel of chitin); if I wanted to the damp chitin could be dried for accumulation until collected enough to utilize. This method should also work for crickets & the soluble components that pass through cloth can be dried if desired.

  • thanks Gringojay, will definitely try it!

  • "Chitosan-based coating with antimicrobial agents: preparation, property, mechanism, and application effectiveness on fruits and vegetables", by Xing, et al (2016) originally published by International Journal of Polymer Science is available on-line as free full pdf from Hidawi downloads.

    Gives good summaries of assorted tactics & reference links for the different specific methods. For those interested in adapting the concepts using relatively low technology see various protocols that combine aloe vera, or lemongrass, or essentials spice oils with chitosan.

  • Before harvest chitosan is also useful for improving food quality. Some examples:

    "Control of latent infection and postharvest main diseases with preharvest chitosan sprays in muskmelons''; abstract only link =

    "Effect of pre-harvest chitosan sprays on post-harvest infection by Botrytis cinerea and quality of strawberry fruit"; free full pdf =

  • Chitin is both part of the insect exo-skeleton & their gut lining. In response to questions about human ingestion of chitin after eating insects here is some good orientation; basically chitin is "good" for most individuals.

    R. Muzzarelli (2010) discusses the "alpha"-chitin form in "Chitins and Chitosans as Immunoadjuvants and Non-Allergenic Drug Carriers", originally published in journal Marine Drugs, Vol. 8(2); free full link =

    In section number 2 " The beneficial activity of chitin as an immunoadjuvant" the interaction of (Quote): " ... chitin stimulates macrophages by interacting with different cell surface receptors such as macrophage mannose receptor, toll-like receptor-2 ..., C-type lectin receptor Dectin-1, and leukotriene 134 receptor ...." The report discusses more details for those interested, a general inference is that chitin enhances engagement of Th1 immunological dynamics & limits Th2 immunogical reactions.

    DaSilva, et al. (2009) has a "Chitin Is a Size-Dependent Regulator of Macrophage TNF and IL-10 Production", originally published in the Journal of Immunology", Vol.182(6); free full text =

    Quote: " ...different sized chitin fragments ... activate distinct signaling pathways that differentially regulate the production of TNF and IL-10 ...(&)... TLR2 activation ... decrease Th2 inflammation ...." The issue of chitin fragment size can be stated as our mammal chitin-ase enzyme (for most people) cleaving ingested bug chitin into the "right" size.

  • Anyone wondering whether there are commercial options other than rearing insects for edible products may find the following an easier program. It bypasses issues of standardizing their diet, timing of life cycles to match sales & government food regulations. Also, in response to those wondering about cockroach utilization options, in general their wings = ~19% chitin, & dorsal thorax/ventral thorax/antennae/cerci = ~25-29% chitin, & head/pronotum/abdomen/legs associated exo-skeleton = ~ 30-37% chitin.

    Pupal (as well as larval) insect chitin extraction & also it's conversion to chitosan was presented at the Bangkok 1997 Asia Pacific Chitin & Chitosan Symposium by A.Haga's "Preparation of chitin from thin-shelled cocoons with pupa obtained as waste from the silk reeling process". Although yields are specific to the bug used the concept likely (?) can be extrapolated to other common pupae.

    Haga's experiments using different proportions of chemical agents to 1st strip protein out of the chitin by boiling (100 Celsius) in 0.75-2.5 N NaOH (ideal return was with a concentration of 1 Mole NaOH) for 42 hours duration. In the event anyone trying to use this method determines they require further de-proteination another tactic is to then take the previously treated chitin & give it 20 hours immersion in 0.4% Na2CO3.

    After (2nd) de-proteination the removal of minerals was performed at 25 Celsius (to avoid high temperature inducing acid hydro-lysis of the chitin) using 1.0 - 2.0 N HCL (ideal return was with a concentration of 2 Mole HCL ) for 96 hours duration. Haga's ideal ratio of reagent, temperature & time yielded 33% chitin from the raw silkworm pupae/larvae material.

    Chitosan elaboration begins after the isolation of chitin & Haga removed some of the melanin color by soaking in alcohol (96-99% EtOH) for 4 hours duration. In the event anyone trying de-colorize (remove melanin residual pigment) the chitin has no pure alcohol available another tactic is to use hydrogen peroxide (H2O2) for 1 hour duration stewing at below boiling temperatures (ideally 7 75-80 Celsius).

    Formation of chitosan structure requires moving acetyl groups from their molecular position in chitin matrix; the amount (degree) of acetyls removed (de-acetylation) is variable depending on method. Haga, found subjecting his colorless silkworm derived chitin to 12.5 Mole NaOH concentration at 150 Celsius for a duration of 16 hours produced just under 38% chitosan from chitin. Although I have no data for Haga's chitosan degree of acetylation my assumption is it would be at least 70% de-acetylated chitosan using this method.

    Later (2000) Haga teamed up with Zhang, et al. on "Structure of insect chitin isolated from beetle larva cuticle and silkworm (Bombyx mori) pupa exuvia"; abstact link = . Having perfected methodology somewhat they report "... N-deacetylation of insect chitin ... easier than ... crustaceous chitin, and about 94% of the N-acetyl groups were removed in one treatment with 40% NaOH for 4 h at 110°C."

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