Personal fat threshold: How to create a diabetic
An interactive tool showing how diabetes happens.
What does this mean?
Remember that fat and carbohydrates are fuel. If we take in more fuel than we need, we store it in the fuel tanks: fat cells, and glycogen stores in the liver and muscle.
We tend to think of type 2 diabetes as just a “sugar problem,” but how we handle excess fuel matters too. Glycogen is stored sugar in the liver and muscle. These reserves are limited and refill after we eat. With continued excess intake, carbohydrate can be turned into fat, and the body can also store more of the fat we eat. If healthy fat storage becomes strained, fat can accumulate in tissues and interfere with insulin. Blood sugar rises when insulin can no longer keep up and the liver releases too much glucose. Limited healthy fat storage can therefore help drive type 2 diabetes.
People differ in how much fat they can store under the skin without metabolic strain. Genetics help shape that capacity. Some people can keep expanding that tank for a long time. For others, even a modest weight gain can matter.
The slider is a model of that overflow—not your personal threshold. First, watch glycogen replenish in the liver and muscle. Then the model focuses on increasing pinchable fat under the skin. As healthy storage comes under strain, more fat can accumulate around the organs as visceral fat, and within the liver, pancreas, and muscle. In real life these processes overlap; they do not have to fill one at a time. Full glycogen stores are normal and do not themselves cause diabetes. If insulin can no longer keep up, glucose stays elevated in the blood, often alongside higher circulating fats. That can lead to type 2 diabetes.
This is not type 1. Type 1 usually involves autoimmune destruction of the cells that make insulin, leaving the body unable to make enough insulin. Different disease.
Choose a threshold, then slide upward to add fuel: glycogen first, followed by fat accumulation in this teaching sequence. Higher thresholds delay glucose changes in this fictional example. The scale is not time, calories, or pounds.
A fuller body and more fat stored under the skin before the internal changes rise. Fictional example; body size does not identify a personal threshold.
This three-dimensional teaching model separates generalized fat under the skin from visceral fat inside the abdomen. It is not a patient scan or a prediction of an individual person's body shape.
Move the lever upward to add fuel. Teal = glycogen · HbA1c and storage levels are illustrative, not personal predictions.
What this stage means & how to read the views
Liver and muscle hold glucose as glycogen. This example starts with partly stocked reserves. Move the slider to watch the teal glycogen highlights build before added fat appears.
Replenishing glycogen is normal. It is not a step into diabetes.
Extreme threshold / hyperplasia. Adipocyte hyperplasia adds fat cells that can store energy. This helps explain why a person with substantial obesity may not have diabetes. This is a possible phenotype, not a guarantee of lasting protection or absence of other health risks. The cell counts are schematic.
The outer layer grows with fat under the skin; moderate visceral fat also rounds the abdomen from the inside.
HbA1c reflects average glucose over about 3 months. This readout is a fictional example assuming sustained levels, not an estimate from body fat.
Teal highlights = glycogen. Stored carbohydrate in liver and muscle; levels are illustrative.
Body arteries are shown through tissue. Glucose and lipid symbols are enlarged; counts are illustrative.
The pale abdominal muscle wall separates outer subcutaneous fat from deep visceral fat. Fat is dark on CT; added colors identify compartments. A larger belly can reflect both types of fat and does not diagnose diabetes.
Fuel storage overlaps. Glycogen replenishment, fuel use, and fat storage can happen together. Fat under the skin, around organs, and within organs can also increase together.
Diabetes is diagnosed with blood tests. Type 2 can develop when insulin production cannot meet the body’s needs. The slider cannot diagnose or predict it.
About the model & sources
About the abdominal views. These are CT-style teaching diagrams, not patient scans or measured segmentations. The muscle wall separates subcutaneous fat from the deep abdominal compartment. Fat is darker than muscle on CT; gold, orange, and purple overlays identify the modeled compartments. The baseline stays fixed and the current view uses the same field of view. The drawing approximates upper-abdominal relationships rather than reproducing an exact scan level. Added visceral fat drives the deeper expansion here. The standing figure’s organs retain their original dimensions, while fat grows around them. Intra-organ fat changes tissue appearance, not organ size. The CT-style rendering uses darker fat, varied soft-tissue shading, irregular bowel loops, renal detail, and cortical and trabecular bone to approximate imaging appearance. Both subcutaneous and visceral fat can increase waist size. Neither body shape nor this diagram determines an individual’s fat distribution or diabetes status. Reference anatomy: Undergraduate Diagnostic Imaging Fundamentals: Abdomen. No patient-scan pixels are used in this procedural teaching view. See NIDDK: Body fat distribution and health risks.
About the rotatable 3D figure. This build uses the adapted Z-Anatomy geometry and Three.js renderer from the supplied Body Composition V8 app. Fat + muscle shows a gradually expanding outer subcutaneous layer over named anatomical muscles. A separate visceral control expands the abdominal wall and the actual omental and mesocolic meshes. Inside abdomen provides a teaching cutaway of the liver, pancreas and bowel. The geometry is anatomical reference material; regional fat deformations, color changes and stage timing remain illustrative rather than patient measurements. Glycogen is retained in the reserve meters and original 2D fallback. This model cannot determine individual organ-fat volume, diabetes risk or remission from body shape.
About glycogen. Glycogen is a reserve of stored glucose in liver and muscle. The liver can use it to support blood glucose; muscle uses its own glycogen for activity. These reserves are limited and change with meals and movement. See NCBI Bookshelf: Glycogenolysis. Carbohydrate can also be converted into fat during sustained excess intake, as examined in a human carbohydrate-overfeeding study. The glycogen-first segment is a teaching sequence, not a requirement that glycogen must be full before any fat can be stored. Its teal highlights and partially stocked starting bars are illustrative; glycogen is not visibly teal. High blood glucose reflects impaired regulation and insufficient insulin, not simply full storage tanks.
The heart is visible within the chest, with coronary arteries supplying its surface. The added surface fat is called epicardial fat; it grows with the visceral-fat example here. The baseline artwork already shows a small normal layer. This is an illustration of where fat can accumulate, not an additional diabetes threshold. Heart position and coronary connections follow OpenStax: Heart Anatomy.
The major arteries are shown through the tissues in a simplified front-view projection. Aortic-arch branches and limb pathways follow OpenStax: Circulatory Pathways. Glucose and lipid symbols are enlarged to show the changing concentration; they are not artery-blocking clots or plaque.
The personal fat threshold is a hypothesis about individual susceptibility to excess fat and type 2 diabetes. Fat under the skin (subcutaneous fat) can act as an energy reservoir. Limited healthy storage may contribute to fat accumulating around organs (visceral fat) and in tissues such as the liver and pancreas. The ReTUNE study supports the concept in people with type 2 diabetes at a lower BMI.
The numbered fat-storage marks organize the explanation; they are not established clinical thresholds or a universal sequence. Fat-depot shapes expand over one anatomical image. Added visceral tissue is rendered as one continuous abdominal fat bed behind a smaller organ core, while the outer abdominal fat layer moves outward. Organs and limbs are never stretched. Whole-body images do not crossfade. Every curve, body-shape change, and particle count is illustrative. Bar lengths compare a tissue with its own displayed range, not the quantity of fat in different tissues. A full bar means the end of this animation’s range, not a full organ.
Fat tissue can expand by enlarging existing cells (hypertrophy) and forming new cells from precursors (hyperplasia). Recruitment varies by fat depot; a human overfeeding study observed new fat-cell formation in lower-body fat. Extreme is a fictional high-capacity example, not a clinical category, and hyperplasia is not exclusive to it. Its controlled glucose does not imply unlimited safe storage: metabolically healthy obesity still carried increased future diabetes risk in the Whitehall II study. There is no validated “hundreds of pounds” cutoff in this model.
Insulin resistance and insulin-producing beta-cell function both matter. Extra circulating fats can appear before high blood glucose. Glucose rises because its regulation is impaired, not because it is physically squeezed out of fat stores. Muscle fat is not always harmful; trained athletes can store fat in muscle while remaining insulin sensitive. Fat loss can improve metabolic health, but moving this slider backward does not predict diabetes remission.
About HbA1c. The NIDDK A1C guide defines the prediabetes range as 5.7–6.4% and the diabetes range as 6.5% or above. HbA1c reflects average glucose over approximately 3 months. This model assigns fictional sustained-glucose examples to the slider; it cannot estimate a person's HbA1c, and moving it is not an immediate biological change. The number is rounded to one decimal and the label follows that displayed value. The chosen starting value is 4.0% for every preset. The chosen endpoints are about 10.1% for Lower, 8.4% for Moderate, 7.0% for Larger, and 5.2% for Extreme; these illustrate contrasting scenarios, not typical outcomes for people with those body shapes. A diabetes diagnosis usually requires confirmation with another test.
Type 1 and type 2 have different mechanisms: see NIDDK: Symptoms & Causes of Diabetes.
- Individual susceptibility and body size: Taylor & Holman, personal fat threshold hypothesis, Clinical Science (2015).
- Personal threshold and lower BMI: Taylor et al., ReTUNE study, Clinical Science (2023).
- Fat distribution and variable responses to fat gain: Johannsen et al., overfeeding study, Diabetes Care (2014).
- Insulin resistance and rising blood glucose: NIDDK: Insulin Resistance & Prediabetes.
3D anatomy source & stage timing
3D anatomy and sequencing. This build reuses the exact muscle, skeleton, outer-body and digestive-organ mesh files embedded in your Body Composition V8 app, plus its Three.js-based renderer. Adapted Z-Anatomy meshes (Gauthier Kervyn, Marcin Zielinski, Lluís Vinent and contributors), derived from BodyParts3D / The Database Center for Life Science; adapted meshes remain CC BY-SA 4.0. Anatomy source · Asset license. Regional deformations, colors, cutaway windows and teaching-stage timing are modifications, not measured patient fat compartments. The added subcutaneous layer starts after the glycogen prelude; added visceral tissue begins at the Around organs marker, with later organ-fat stages. Baseline visceral tissues remain present. Real fat depots can change concurrently, and appearance cannot identify a person's fat threshold, organ fat, HbA1c or likelihood of remission. The fixed Normal CT remains the original reference; Current CT and 3D use shared added-fat controls, not co-registered patient scans.